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YR2: Immunology > Hypersensitivity and Allergy > Flashcards

Hypersensitivity and Allergy Flashcards

1
Q

What are hypersensitivity reactions usually mounted against?

A

Harmless foreign antigens (allergy)
Autoantigens (AI disease)
Alloantigens (Graft rejection)

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2
Q

What are the 4 types 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

1st exposure: sensitisation: IgE is produced, which binds to mast cells + basophils
2nd exposure: antigen cross-links the IgE on mast cells causing degranulation + release of inflammatory mediators

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4
Q

Give examples of Type 2 hypersensitivity diseases

A

Organ specific AI diseases: myasthenia gravis, glomerulonephritis, pemphigus vulgaris, pernicious anaemia
AI cytopenias: AI 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, activate complement + cause cell recruitment + activation
Can cause tissue damage e.g. SLE

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6
Q

3 examples of diseases caused by Th1 cell mediated delayed type hypersensitivity.

A

Chronic graft rejections
Graft-versus-host disease
Coeliac disease

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7
Q

Describe the mechanism of Th1 and cytotoxic T cell mediated delayed type hypersensitivity.

A

Transient/ persistent antigen is presented to T cells, which then activate macrophages + CTLs
Activated macrophages produce TNF-alpha, which is responsible for much of the tissue damage

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8
Q

What are 3 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)

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

Common ~50% of YAs in the UK

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12
Q

Genetic risk factors of atopy

A

~80% of atopics have a family history

Genetic component is polygenic but genes of IL-4 cluster + 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 4 other environmental factors affect atopy?

A

Family size (higher in small families)
Infections (early life infections protect)
Animals (early exposure protects)
Diet

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16
Q

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

A

Type 1 hypersensitivity

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17
Q

What type of hypersensitivity is responsible for chronic urticaria?

A

Type 2 hypersensitivity

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18
Q

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

A

Type 1 + type 4 hypersensitivity

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19
Q

Describe sensitisation in atopic airway disease.

A

Naive T cells are exposed to the antigen by APCs
Differentiate into: Th1 cells (producing IFN-gamma), T regs or Th2 cells
Th2 cells produce IL4 +13 leading to B cell activation
B cells differentiate into plasma cells which produce IgE antibodies specific to antigen

20
Q

Describe what happens in 2nd exposure to the allergen in atopic airway disease

A

Allergens are presented by APCs to memory Th2 cells, which release IL-5, causing eosinophil degranulation
Th2 cells also release IL-4 + IL-13, which stimulate production of IgE by plasma cells
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 eosinophils.

A

Bi-lobed nucleus

Contains large granules of toxic proteins

23
Q

What receptors do mast cells have on their cell surface? What does cross linking of these receptors result in?

A

IgE receptors

Mediator release

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? Describe the appearance of neutrophils

A

55-60%
Multi-lobed nucleus
Granules containing digestive enzymes

26
Q

What 3 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 bronchi

27
Q

Describe 5 changes seen in a patient with chronic asthma.

A

Airway lumen is narrowed + wall is grossly thickened:
Cellular infiltration by Th2 lymphocytes + eosinophils
Smooth muscle hypertrophy
Mucus plugging
Epithelial shedding
Subepithelial fibrosis

28
Q

State 6 important clinical features of asthma.

A 
Chronic episodic wheeze 
Bronchial hyper-responsiveness  
Cough 
Mucus production  
Breathlessness  
Reduced + variable peak expiratory flow (PEF)
29
Q

What can allergic eczema lead to sensitisation of?

A

House dust mites: their proteins can penetrate dry, cracked skin

30
Q

3 symptoms of a mild reaction to a food allergy

A

Itchy lips + mouth
Angioedema
Urticaria

31
Q

4 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 5 symptoms of anaphylaxis.

A 
Itchiness around mouth, pharynx + lips  
Swelling of the lips + throat  
Wheeze, chest tightness, dyspnoea 
Faintness, collapse  
Diarrhoea + vomiting
35
Q

How can you test for allergies?

A

Skin prick test

36
Q

What is the emergency treatment of anaphylaxis?

A

EpiPen + kit
Adrenaline
Antihistamine
Steroid

37
Q

Describe the step-by-step treatment of asthma.

A

Step 1: short acting B-2 agonist (e.g. salbutamol)
Step 2: low-moderate dose inhaled steroids (e.g. beclomethasone)
Step 3: add long acting bronchodilators or a leukotriene receptor antagonist + high dose inhaled steroids
Step 4: add courses of oral steroids

38
Q

What are the 2 types of immunotherapy that are used to develop tolerance in patients?

A 
Subcutaneous immunotherapy (SCIT) 
Sublingual immunotherapy (SLIT)
39
Q

What common feature is present in all hypersensitivity reactions? What causes this and what are the clinical signs?

A 
Inflammation 
Vasodilation causes increased blood flow
Increased vascular permeability
Inflammatory mediators + cytokines
Inflammatory cells + tissue damage
Redness, Heat, Swelling, Pain
40
Q

List 4 diseases where type 1 sensitivity plays a key role

A

Anaphylaxis
Asthma
Rhinitis
Food allergy

41
Q

What are the 4 most commonly effected tissues in type 3 hypersensitivity reactions?

A

Renal
Skin
Joints
Lung

42
Q

Which hypersensitivity states are neutrophils particularly important in?

A

Virus induced asthma
Severe asthma
Atopic eczema

43
Q

List 4 symptoms of allergic rhinitis

A

Sneezing
Rhinorrhoea
Itchy nose + eyes
Nasal blockage, sinusitis, loss of smell/ taste

44
Q

What are 3 treatment options for allergic rhinitis?

A

Anti-histamines
Nasal steroid spray
Cromoglycate

45
Q

What are the treatment options for eczema?

A

Emollients

Topical steroid cream

YR2: Immunology (5 decks)

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