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2. CP - Core Immunology > (10) Allergic Diseases > Flashcards

(10) Allergic Diseases Flashcards

1
Q

What is allergy/hypersensitivity?

A

Undesirable, damaging, discomfort-producing and sometimes fatal reactions produced by the normal immune system (directed against innocuous antigens) in a pre-sensitised (immune) host

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2
Q

How many immunopathological classifications are there for allergy?

A

4 types - Coombs and Gell 1963

type 5 - extended classification

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3
Q

What are the 4 types of hypersensitivity?

A

type 1 = anaphylactic

type 2 = cytotoxic

type 3 = immune complex

type 4 = delayed type

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4
Q

Which antibodies are involved in the 4 types of hypersensitivity?

A

type 1 = IgE

type 2 = IgG, IgM

type 3 = IgG, IgM

type 4 = none

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5
Q

What is the immunopathogenesis in type II cytotoxic?

A

IgG/IgM Ab response against combined self/foreign antigen at the cell surface - complement activation/phagocytosis/ADCC

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6
Q

What are the clinical features of type II cytotoxic?

A
  • onset minutes to hours

- cell lysis and necrosis

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7
Q

What are the common antigens of type II cytotoxic?

A

Penicillin

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8
Q

What are the associated diseases of type II cytotoxic?

A
  • erythroblastosis fetalis

- goodpasture’s nephritis

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9
Q

What are the steps when penicillin causes a type II cytotoxic reaction to cause lysis?

A
  • complement-coated penicillin-modified red blood cells are phagocytosed by macrophages using their complement receptors
  • macrophages present peptides from the penicillin-protein conjugate and activate specific CD4 T cells to become TH2 cells
  • B cells are activated by the antigen and by help from activated TH2 cells
  • Plasma cells secrete penicillin-specific IgG which binds to modified red blood cells
  • complement lytic pathway
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10
Q

What is the immunopathology in type III-immune complex reactions?

A

IgG/IgM Ab against soluble antigen-immune complex deposition

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11
Q

What are the clinical features of type III-immune complex reactions?

A
  • onset 3-8 hours

- vasculitis

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12
Q

What is the traditional cause of type III-immune complex reactions?

A

Serum sickness

Mouldy hay – farmer’s lung

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13
Q

What disease is associated with type III-immune complex reaction?

A

SLE

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14
Q

If the site of immune-complex deposition is the blood vessel walls, what is the resulting disease?

A

Vasculitis

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15
Q

If the site of immune-complex deposition is the renal glomeruli, what is the resulting disease?

A

Nephritis

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16
Q

If the site of immune-complex deposition is the joint spaces, what is the resulting disease?

A

Arthritis

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17
Q

If the site of immune-complex deposition is the perivascular area, what is the resulting disease?

A

Arthus reaction

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18
Q

What is arthus reaction?

A

The Arthus reaction is a type of local type III hypersensitivity reaction which involves the deposition of antigen/antibody complexes mainly in the vascular walls, serosa (pleura, pericardium, synovium) and glomeruli.

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19
Q

If the site of the immune-complex deposition is the alveolar/capillary interface, what is the resulting disease?

A

Farmer’s lung

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20
Q

What is the immunopathology in type IV-delayed reactions?

A

Antigen specific T-cell mediated cytotoxicity

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21
Q

What are the clinical features of type IV-delayed reactions?

A
  • delayed onset 48-72 hours

- erythema induration

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22
Q

What is the common antigen in type IV-delayed reactions?

A
  • metals eg. Nickel

- (tuberculin reaction)

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23
Q

What disease is associated with type IV-delayed allergic reaction?

A

Contact dermatitis

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24
Q

In type IV-delayed allergic reactions, an antigen leads to a T cell response, briefly describe the following steps

A
  • antigen is processed by tissue macrophages and stimulates THI cells
  • chemokines, cytokines and cytotoxins are released which perform different functions
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25
Q

In type IV-delayed allergic reactions, chemokines, cytokines and cytotoxins are released. State which and their functions

A
  • chemokines = macrophage recruitment to the site of antigen
  • IFN-y = activates macrophages increasing release of inflammatory mediators
  • TNF-a and TNF-b = local tissue destruction, increased expression of adhesion molecules on local blood vessels
  • IL-3/GM-CSF = monocyte production by bone marrow stem cells
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26
Q

Describe the stages in the development of allergy

A
  • environment and genetics (atopy)
  • barrier dysfunction
  • sensitisation
  • changes in T cell sub-sets dominated by Th2
  • IgE
  • ALLERGY
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27
Q

Which allergy is associated with the eyes?

A

Allergic conjunctivitis

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28
Q

Which allergy is associated with the nose?

A

Allergic rhinitis

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29
Q

Which allergy is associated with the mouth?

A

Oral allergy syndrome

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30
Q

Which allergy is associated with the airways?

A

Allergic asthma

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31
Q

Which allergy is associated with the skin?

A

Atopic dermatitis

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32
Q

Which allergy is associated with the GI tract?

A

Food allergy

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33
Q

How do we get allergies?

A
  • those components of the immune system involved in responses to parasitic infection are also involved in allergic responses
  • the system has developed to produce a rapid tissue-based response to re-infection
  • the lack of infectious drive is a contributory factor in allergic disease
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34
Q

In immune response to parasitic disease, what is there increased levels of?

A

Increased levels of IgE

  • total
  • specific to pathogen – cross-reactive
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35
Q

In immune responses to parasitic diseases, there is tissue inflammation with what?

A
  • eosinophilia and mastocytosis

- basophil infiltration

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36
Q

What is eosinophilia?

A

An increase in the number of eosinophils in the blood, occurring in response to some allergens, drugs, and parasites, and in some types of leukaemia

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37
Q

Which cells are present in immune responses to parasitic disease?

A

Presence of CD4+ T cells secreting: IL4, IL5, IL13

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38
Q

Describe the ‘hygiene hypothesis’ in relation to parasitic disease and allergy

A
  • stimulation by microbes is protective
  • animal models – T1DM, EAE, asthma
  • increased atopy (asthma) after anti-parasitic Rx
  • prevention of autoimmunity (Crohn’s) by infections
  • pro-biotics in pregnant women
  • mechanism – Th1 Th2 deviation
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39
Q

What are the genetic influences on the ‘allergic’ immune response?

A
  • polygenic disease
  • cytokine gene cluster IL3, IL, IL9, IL13
  • IL12R; IL4R
  • FceRI
  • IFNg; TNF
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40
Q

Are genetic influences of ‘allergic’ immune response sufficient for disease?

A

No, not sufficient for disease, only susceptibility

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41
Q

What defects causing an allergic response can be caused by genes?

A
  • barrier function
  • tissue response
  • atopic immune responses
  • environment sensing
  • eosinophils
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42
Q

Which genes contribute to all of asthma, atopic dermatitis and allergic rhinitis?

A

C11orf30

LRRC32

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43
Q

Which genes contribute to only allergic rhinitis?

A

TLR6

NOD1

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44
Q

Which gene contributes to both asthma and allergic rhinitis?

A

TSLP

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45
Q

What is an allergen?

A

Antigens that initiate an IgE-mediated response

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46
Q

What does the first encounter with an allergen result in?

A

Innate and IgM response (you do not generate and allergic response on first encounter)

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47
Q

What is the conventional immune response?

A
  • allergen requires processing
  • presentation to T cells and cytokine release
  • results in delineation of T-helper subsets into different types
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48
Q

In allergic responses, what are the early priming events?

A
  • decreased barrier function
  • allergen is passively taken in or actively taken up through barrier
  • immature dendritic cell gets activated
  • dendritic cell migrates and matures
  • mature dendritic cell presents antigen to naive T cell in lymph node
  • T cell activation
  • Th2-cell development
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49
Q

What is a dendritic cell?

A

Antigen-presenting cell

Main function is to process antigen material and present it on the cell surface to T cells

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50
Q

In an allergic response there is differentiation of T-helper cells. Give 4 different types of T helper cell involved

A
  • Th1
  • Th2
  • Th17
  • Treg
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51
Q

What do Treg cells do?

A

Regulatory T cells calm down the immune response. They cause inflammatory suppression caused by the other T helper cells

52
Q

Which effector cytokines do Treg cells release?

A
  • IL-10

- TGFb

53
Q

Which effector cytokines do Th1 cells release?

A
  • IFN-y

- IL-2

54
Q

Which effector cytokines do Th2 cells release?

A
  • IL-4
  • IL-5
  • IL-13
55
Q

Which effector cytokines do Th17 cells release?

A
  • IL-17
  • IL-21
  • IL-22
56
Q

How are IgE antibodies produced?

A

Th2 cells release IL-4 cytokines which stimulates the B cells to proliferate and produce IgE

57
Q

Which cell is ultimately responsible for IgE production?

A

B cells

58
Q

Which T cell is involved in IgE production?

A

Th2

59
Q

Which cytokines is involved in IgE production?

A

IL-4

60
Q

How do IgE antibodies go on to produce an allergic response? (type I allergic response)

A
  • IgE binds to the Fc receptor on sensitised mast cells
  • mast cells activation and degranulation
  • release of mediators which cause the symptoms
61
Q

Which parts of the body are affected by the vasoactive amines/lipid mediators/chemokines/cytokines released by mast cells and basophils?

A
  • smooth muscle
  • blood vessels
  • platelets
  • sensory nerve endings
  • eosinophils
62
Q

What is the immunopathogenesis in IgE mediated allergic response?

A

IgE antibody mediated mast cell and basophil degranulation - release of pre-formed and de novo synthesised inflammatory mediators

63
Q

What are the clinical features of IgE mediated allergic response?

A
  • fast onset (15-30 minutes)
  • wheal and flare

(unlikely to be this allergy if presents the day after)

64
Q

What are the two types of response in IgE mediated allergic responses?

A
  1. initial response/immediate phase

2. late-phase reaction

65
Q

What is involved in the initial response in IgE mediated allergic responses?

A
  • degranulation of mast cells and basophils
  • granule contents = histamine, proteases, chemotactic factors

(primary mediators)

66
Q

What is involved in the late-phase reaction in IgE-mediated allergic responses?

A

Arachidonic pathway

  • secondary mediators
  • leukotrienes and prostaglandins
  • eosinophils
  • central role for Th2 T cell
67
Q

What is the role of the Th2 T cell?

A
  • multiple cytokine release
  • innate inflammatory response (macrophages etc)
  • drive for immunoglobin production (support for B cells)
68
Q

What are the 3 conditions in the atopic triad?

A
  • asthma
  • rhinitis
  • eczema
69
Q

Which of the atopic triad are type I hypersensitivity?

A
  • asthma

- rhinitis

70
Q

Which of the atopic triad are type IV hypersensitivity?

A
  • eczema
71
Q

What are the symptoms of allergic rhinitis caused by mast cells in the nasal mucosa and airway epithelium?

A
  • nasal congestion (oedema, mucus, nasal polyps)
  • nasal inflammation
  • tonsillar and adenoidal enlargement
72
Q

What are the symptoms of asthma caused by mast cells in the airway epithelium and lungs?

A
  • airway inflammation (oedema, mucus)

- airway constriction and hyper-reactivity

73
Q

What are the two types of rhinitis?

A
  • allergic

- non-allergic

74
Q

What are the two types of allergic rhinitis?

A
  • perennial

- seasonal

75
Q

What allergens can cause rhinits?

A
  • house dust mite
  • animal danders
  • pollens
76
Q

What are the symptoms of rhinitis?

A
  • blocked nose
  • runny nose
  • often with eye symptoms
77
Q

What is the treatment for rhinitis?

A
  • antihistamines

- nasal steroids

78
Q

What is asthma a disease of?

A

Inflammation and hyper-reactivity of the small airways

79
Q

Which allergens cause asthma?

A
  • aero-allergic stimuli in childhood (airborne allergens)

- house dust mite - key pathogenic importance

80
Q

What are the immediate symptoms of asthma due to?

A

IgE mediated

81
Q

What is damage to the airways in asthma caused by?

A

Late phase reaction

82
Q

Damaged airways in asthma are hyper-reactive to what?

A

Non-allergic stimuli eg. fumes

83
Q

What is the basic difference between asthma and rhinitis?

A 
Rhinitis = upper airways
Asthma = lower airways
84
Q

What is the pathogenesis in asthma? (describe the inflammatory cascade in allergic asthma)

A
  • allergen
  • antigen-presenting cell
  • Th2 cell
  • IL-4 and IL-3 to B cell plasma cell
  • IL-5 to eosinophil
  • B cell plasma cells produces IgE
  • IgE to mast cells and basophils
  • mast cells, basophils and eosinophils cause release of histamine, leukotrienes, prostaglandins, cytokines, basic proteins and enzymes
  • allergic asthma
85
Q

What are the two major types of dermatitis?

A
  • atopic

- contact (allergic/non-allergic)

86
Q

What is atopic dermatitis also known as?

A

Atopic eczema

87
Q

How would a patient with atopic dermatitis present?

A
  • intense itching
  • blistering/weeping
  • cracking of skin
88
Q

What is a major trigger in atopic dermatitis?

A

House dust mite

89
Q

What is the treatment for atopic dermatitis?

A
  • topical steroids

- moisturisers

90
Q

Which cytokine mediator causes the scratch/pruritus in atopic dermatitis?

A

IL-31 directly causes scratch

91
Q

How is there a viscous circle in atopic dermatitis?

A

Barrier disruption leads to development of Th2 then IgE and also T cell-derived itch mediator: IL-31

This causes pruritus/scratch

The scratching causes further barrier disruption and therefore more IL-31 and more scratching

92
Q

What is anaphylaxis?

A

An acute, potentially life-threatening, IgE-mediated systemic hypersensitivity reaction

93
Q

What are the 3 classifications of anaphylaxis?

A
  • 1 (mild)
  • 2 (moderate)
  • 3 (severe)
94
Q

What are some symptoms of type 1 (mild) anaphylaxis?

A
  • pruritus
  • abdominal pain
  • nausea and vomiting
  • runny nose and sneezing
  • throat tightness
  • mild wheezing
  • tachycardia (>15 beats per min)
  • increased anxiety
95
Q

What are some symptoms of type 2 (moderate) anaphylaxis?

A
  • angioedema
  • severe abdominal pain
  • dysphagia
  • hoarseness
  • moderate dyspnoea
  • tachycardia (>15 beats per min)
  • light-headedness
  • feel of pending life-threatening event
96
Q

What are some symptoms of type 3 (severe) anaphylaxis?

A
  • profuse diarrhoea and loss of bowel control
  • severe wheezing
  • sao2
97
Q

What are the methods of diagnosis of allergy?

A
  • history
  • specific IgE (>0.35 KuA/L)
  • skin prick test (>3mm wheal)
  • intra-dermal test
  • oral challenge test
  • basophil activation test
  • component resolved diagnostics
98
Q

What is the gold standard test in allergy diagnosis?

A

Oral challenge test

eg. feed peanut and see what happens (quick onset)

99
Q

Why is history important in allergy diagnosis?

A

Temporal relationship between exposure and symptoms is relevant

Type 1 = symptoms are short-lived

100
Q

How do you measure IgE in allergy diagnosis?

A

Blood sample

BUT can have positive test and be clinically tolerant

101
Q

How is a skin prick test carried out in allergy diagnosis?

A

EG.

negative control = drop of saline solution on skin

positive control = drop of histamine on skin

then eg. drop of grass pollen on skin

and see if you have a reaction

102
Q

What happens in chronic spontaneous urticaria?

A

Random rashes for no reason

103
Q

How does the basophil activation test work in allergy diagnosis?

A

Certain substances (makers) inside the basophil cell either come out of the cell or increase in number when the cell is activated

eg. CD63 comes out of the cell

104
Q

What are the advantages and disadvantages of the specific IgE test in allergy diagnosis?

A

Advantage = safe (just a blood test)

Disadvantage = false negatives and false positives

105
Q

What are advantages and disadvantages of the skin prick test in allergy diagnosis?

A

Advantage = quick (don’t have to send samples to lab) and patient satisfaction

Disadvantages = false negatives, false positives, antihistamines, slight risk

106
Q

What are the symptomatic treatments for allergy?

A
  • antihistamines
  • steroids
  • adrenaline
107
Q

What specific treatment is there for allergy?

A

Immunotherapy - modulate immune system (subcutaneous or sublingual administration)

108
Q

What are the indications for immunotherapy for allergy?

A
  • life threatening reactions to wasp and bee sting
  • severe hay fever
  • animal dander allergy
109
Q

Immunotherapy for allergy is not helpful in which situations?

A
  • multiple allergies
  • food allergy
  • allergic rashed eg. eczema, urticaria
110
Q

Describe the mechanism of immunotherapy

A
  • more Th1 and less Th2 in tissues

- decreased IgE and more of other types of antibodies (IgG, IgA) and so more competition

111
Q

What are the major food allergens?

A
  • cow’s milk
  • egg
  • legumes (peanut, soybean, tree nuts)
  • fish
  • crustaceans/molluscs
  • cereal grains
112
Q

The major food allergens are what type of proteins?

A

Water-soluble glycoproteins 10-60kd

113
Q

What are the clinical manifestations of food allergy?

A

Gastrointestinal

  • vomiting
  • diarrhoea
  • oral symptoms

Respiratory (upper and lower)

  • rhinitis
  • bronchospasm

Cutaneous

  • urticaria
  • angioedema
  • role of food in atopic dermatitis is unclear

Anaphylaxis

114
Q

Food allergy can be of which 3 types?

A
  • IgE-mediated
  • non-IgE mediated
  • mixed
115
Q

What are some examples of causative agents of IgE mediated type I drug allergy?

A
  • B-lactam antibiotics
  • platinum-based chemotherapeutics
  • perioperative agents
116
Q

What are the clinical manifestations of IgE mediated type I drug allergy?

A
  • urticaria
  • angioedema
  • bronchospasm
  • anaphylaxis
117
Q

What are some examples of causative agents of cytotoxic type II drug allergy?

A
  • penicillin
  • quinine
  • sulfonamides
118
Q

What are the clinical manifestations of cytotoxic type II drug allergy?

A
  • haemolytic anaemia
  • thombocytopenia
  • granulocytopenia
119
Q

What are some examples of causative agents of immune complex type III drug allergy?

A
  • penicillin
  • infliximab
  • thymoglobulin
120
Q

What are the clinical manifestations of immune complex type III drug allergy?

A
  • serum sickness
121
Q

What are some examples causative agents of delayed type type IV drug allergy?

A
  • neomycin
  • glucocorticoids
  • penicillin
  • sulfonamide antibiotics
122
Q

What are the clinical manifestations of delayed type type IV drug allergy?

A
  • contact dermatitis

- exanthems

123
Q

What are the response times in the 4 different types of hypersensitivity?

A

type I anaphylactic = 15-30 minutes

type II cytotoxic = minutes-hours

type III immune complex = 3-8 hours

type IV = 48-72 hours

124
Q

What is the appearance of the 4 different types of hypersensitivity?

A

type I anaphylactic = wheal and flare

type II cytotoxic = lysis and necrosis

type III immune complex = erythema, oedema, necrosis

type IV delayed type = erythema induration

125
Q

What is the histology of the 4 different types of hypersensitivity?

A

type I anaphylactic = basophils and eosinophils

type II cytotoxic = antibody and complement

type III immune complex = complement and neutrophils

type IV delayed type = monocytes and lymphocytes

126
Q

What type of antigens are involved in the 4 different types of hypersensitivity?

A

type I anaphylactic = exogenous

type II cytotoxic = cell surface

type III immune complex = soluble

type IV delayed type = tissues and organs

2. CP - Core Immunology (7 decks)

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