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Y2 MCD Immunology Fwong > 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 
1. Organ specific autoimmune diseases: e.g. Myasthenia gravis (Anti-acetylcholine R Ab)
Glomerulonephritis (Anti-glomerular basement membrane Ab)
Pernicious anaemia (anti-parietal cells Ab)
  1. Autoimmune cytopenias 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 tissues and activate complement and cause cell recruitment
This can cause tissue damage

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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

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7
Q

Describe the mechanism of delayed type hypersensitivity.

A

The transient/persistent antigen is presented to T cells, which then activate macrophage, CTLs and fibroblasts
Activated macrophages produce TNF-alpha, which is responsible for much of the tissue damage

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8
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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9
Q

What is atopy?

A

Atopy means genetic susceptibility to allergic reactions

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10
Q

How common is atopy?

A

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

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11
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 and genes on chromosome 11q have been linked to atopy

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12
Q

Among which age group is atopy most common?

A

Teens

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13
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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14
Q

What other environmental factors affect atopy?

A

Family size, infections, animals, diet

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15
Q

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

A

Type 1 hypersensitivity

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16
Q

What type of hypersensitivity is responsible for chronic urticaria?

A

Type 2 hypersensitivity

17
Q

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

A

Mixed- Type 1 and type 4 hypersensitivity

18
Q

Describe sensitisation in atopic airway disease.

A

T cells are naïve before they have seen their antigen
Once the T cells are exposed to the antigen by APCs, they can become Th1 cells (producing IFN-gamma), T regs or Th2 cells Th2 cells lead to the activation of B cells and the production of IgE antibodies

19
Q

Describe what happens in second exposure to the allergen.

A

In second exposure, the allergens are presented by APCs to memory Th2 cells, which then release IL-5, which causes eosinophil degranulation to release inflammatory mediators.

Inflammatory mediators are also released from Mast cells after binding of allergen to the IgE on mast cell surface + cross linking

Th2 cells also release IL-4 and IL-13, which stimulate MORE production of IgE by plasma cells too.

20
Q

What percentage of blood leukocytes are eosinophils?

A

2-5%

21
Q

Describe the appearance of the nucleus of eosinophils.

A

Bilobed

22
Q

What receptors do mast cells have on their cell surface?

A

IgE receptors

23
Q

What mediators are released by mast cells?

A

Preformed: histamines, cytokines, toxic proteins

Newly synthesised: leukotrienes, prostaglandins

24
Q

What percentage of blood leukocytes are neutrophils?

A

55-60%

25
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

26
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

27
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)
28
Q

What can allergic eczema lead to sensitisation of?

A

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

29
Q

What type of hypersensitivity is food allergy?

A

Type 1 hypersensitivity (IgE)

30
Q

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

A

Itchy lips and mouth
Angioedema
Urticaria

31
Q

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

A

Nausea
Abdominal pain
Diarrhoea
Anaphylaxis

32
Q

What is anaphylaxis?

A

Severe generalised allergic reaction

33
Q

What is anaphylaxis caused by?

A

Generalised degranulation of IgE sensitised mast cells

34
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
35
Q

How can you test for allergies?

A

Skin prick test

36
Q

What is the emergency treatment of anaphylaxis?

A

Adrenaline

37
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 receptorantagonist + high dose inhaled corticosteroids
Step 4: add courses of oral steroids

38
Q

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

A 
Subcutaneous immunotherapy (SCIT) 
Sublingual immunotherapy (SLIT)

Y2 MCD Immunology Fwong (4 decks)

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