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[ ESA 3- Infection and Immunity > Allergies > Flashcards

Allergies Flashcards

1
Q

What does the term hypersensitivity describe?

A

The antigen specific responses that are either inappropriate or excessive, and result in harm to host

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2
Q

What mechanisms underlie the hypersensitivity immune responses?

A

Those employed by the host to fight infections

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3
Q

What are the common features of hypersensitivity responses?

A

Sensitisation phase

Effector phase

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4
Q

What happens in the sensitisation phase of a hypersensitivity response?

A

First encounter with antigen

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5
Q

What happens in the effector phase of a hypersensitivity response?

A

Clinical pathology upon re-exposure to same antigen

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6
Q

What are the types of hypersensitivity reactions?

A

Type I, or immediate
Type II, or antibody mediated
Type III, or immune complex mediated
Type IV, or cell mediated

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7
Q

How quick is the onset of type I hypersensitivity reactions?

A

<30 minutes

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8
Q

What are type I hypersensitivity reactions also known as?

A

Allergies

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9
Q

What are type I hypersensitivity reactions a response to?

A

Environmental non-infectious agents (allergens)

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10
Q

What molecule do type I hypersensitivity reactions involve?

A

IgE

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11
Q

When is the onset of type II hypersensitivity reactions?

A

5-12hrs

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12
Q

What are type II hypersensitivity reactions a response to?

A

Non-soluble tissue antigens

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13
Q

What molecule do type II hypersensitivity reactions involve?

A

IgG

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14
Q

When is the onset of type III hypersensitivity reactions?

A

3-8hrs

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15
Q

What are type III hypersensitivity reactions a response to?

A

Soluble antigens

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16
Q

When is the onset of type IV hypersensitivity reactions?

A

24-48hrs

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17
Q

What is a type IV hypersensitivity reaction a response to?

A

Environmental infectious agents and self antigens

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18
Q

What kind of diseases are type IV hypersensitivity reactions?

A

Autoimmune diseases

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19
Q

What is happening to the worldwide prevalence of allergies?

A

It is increasing

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20
Q

How does the incidence of allergy in the UK compare to other countries?

A

It is in the top 3 countries with the highest incidence of allergy

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21
Q

What % of children in the UK have an allergy?

A

> 50%

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22
Q

How many <45 year olds have 2 or more allergies in the UK?

A

13 million

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23
Q

What proportion of children have a peanut allergy in the UK?

A

1 in 50

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24
Q

How much do allergies cost per year in primary care in the UK?

A

£900 million

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25
Q

What is the development of allergy thought to be affected by?

A

A mixture of genetics and environmental factors

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26
Q

What phenotype often present as non-allergic?

A

TH1

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27
Q

What phenotype often presents as allergic?

A

TH2

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28
Q

How is geographical location related to allergy?

A

Those from developing countries tend to have less allergies, and those from westernised countries tend to have more allergies

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29
Q

Why do people from developing countries tend to have less allergies?

A 
Large family sizes
Rural homes, lifestock
Intestinal microflora variable/transient
Low antibiotic use
High helminths burden
Poor sanitation, high orofecal burden
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30
Q

Why do those from westernised countries tend to have more allergies?

A 
Small family size
Affluent, urban homes
Intestinal microflora stable
High antibiotic use
Low or absent helminths burden
Good sanitation, low orofecal burden
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31
Q

What are the common allergies?

A 
House dust mite, cockroaches
Animals
Tree and grass pollen
Insect venom 
Medicines
Chemicals
Foods
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32
Q

What animals are people commonly allergic too?

A

Domestic pets such as cats and dogs

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33
Q

What insect venoms are people commonly allergic too?

A

Those contained in wasp and bee stings

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34
Q

Give an example of medicines people are commonly allergic too

A

The antibiotic penicillin

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35
Q

Give an example of a chemical people are often allergic too

A

Latex

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36
Q

What foods can people be allergic too?

A 
Milk
Eggs
Wheat
Peanuts
Tree nuts 
Seafood
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37
Q

What should be considered with people with allergies?

A

People with allergies can often have cross-reactions with other associated allergens

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38
Q

What are hypersensitivity reactions caused by?

A

Activation of mast cells through IgE dependant mechanisms

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39
Q

What is the result of activation of mast cells in hypersensitivity?

A

These activated mast cells then release chemical mediators

40
Q

What is the most important chemical mediator in hypersensitivity reactions?

A

Histamine

41
Q

What are the classes of chemical mediators in hypersensitivity reactions?

A 
Enzymes
Toxic mediator
Cytokine
Chemokine
Lipid mediator
42
Q

Give 4 examples of enzyme chemical mediators in hypersensitivity reactions

A

Tryptase
Chymase
Cathpepsin G
Carboxypeptidase

43
Q

What are the biological effects of enzyme chemical mediators in hypersensitivity reactions?

A

Remodel connective tissue matrix

44
Q

Give two examples of toxic mediators in hypersensitivity reactions

A

Histamine

Heparin

45
Q

What are the biological effects of toxic mediators in hypersensitivity reactions

A

Toxic to parasites
Increase vascular permeability
Cause smooth muscle contraction

46
Q

Give 6 cytokine chemical mediators in hypersensitivity reactions

A 
IL-4
IL-13
IL-3
IL-5
GM-CSF
TNF-alpha
47
Q

What are the biological effects of IL-4 and IL-13 in hypersensitivity reactions?

A

Stimulate and amplify TH2 cell response

48
Q

What are the biological effects of IL-3, IL-5, and GM-CSF in hypersensitivity reactions?

A

Promote eosinophil production and activation

49
Q

Where does the TNF-alpha in hypersensitivity reactions come from?

A

Some stored preformed in granules

50
Q

What are the biological effects of TNF-alpha in hypersensitivity reactions?

A

Promotes inflammation
Stimulates cytokine production by many cell types
Activates endothelium

51
Q

What chemokine chemical mediator is released in hypersensitivity reactions?

A

CCL3 (MIP-1alpha)

52
Q

What are the biological effects of chemokines in hypersensitivity reactions?

A

Attracts monocytes, macrophages, and neutrophils

53
Q

Give 4 lipid mediators in hypersensitivity reactions

A

Leukotrienes C4, D4, E4

Platelet-activating factor

54
Q

What are the biological effects of leukotrienes in hypersensitivity reactions?

A

Cause smooth contraction
Increase vascular permeability
Stimulate mucus secretion

55
Q

What are the biological effects of platelet-activating factor in hypersensitivity reactions?

A

Attracts leukocytes
Amplifies production of lipid mediators
Activates neutrophils, eosinophils, and platelets

56
Q

What does an initial exposure to an allergen cause?

A

Plasma cells to create an antigen-specific IgE

57
Q

What happens once an antigen-specific IgE has been produced?

A

It binds to mast cells to sensitise it to the specific antigen (allergen)

58
Q

What does second exposure to an allergen cause?

A

Cross-linking of the IgE molecules on the surface of the mast cell

59
Q

What does cross linking of IgE molecules on the mast cell trigger?

A

The release of granule contents, including histamine and chemokines, and synthesis of new mediators; leukotrienes and prostaglandins

60
Q

What does the release of granule contents from mast cells result in?

A

A number of physiological changes, such as;
Increased vascular permeability
Vasodilation
Bronchoconstriction

61
Q

How is an allergic reaction diagnosed?

A

Blood/serum levels of mast cell products

62
Q

Where can the effects of an allergic reaction manifest?

A

The epidermis

Deep dermis

63
Q

How can the effects of allergic reaction manifest in the epidermis?

A

Increased vascular permeability and vasodilation results in urticaria (hives)

64
Q

How does urticaria present?

A

Creates a wheal and flare type marking on the skin

65
Q

How can the effects of an allergic reaction manifest in the deep dermis?

A

Increased vascular permeability and vasodilation results in angiodema of the lips, eye, tongue, and upper respiratory tract

66
Q

What is the problem with the manifestation of allergic reaction in the deep dermis?

A

It can carry the risk of suffocation if in the respiratory tract

67
Q

What can systemic activation of mst cells result in?

A

Anaphylaxis

68
Q

How serious is anaphylaxis?

A

Medical emergency- death if not treated

69
Q

What happens in anaphylaxis?

A

Increased vascular permeability leads to hypotension and cardiovascular collapse
Generalised urticaria and angiodema
Bronchoconstriction leads to breathing problems

70
Q

How many deaths did anaphylaxis result in between 1992 and 2001?

A

Over 200 but im pretty sure this isnt going to be in the exam so its a pointless fact

71
Q

When should anaphylaxis be treated?

A

Immediately

72
Q

How should anaphylaxis be treated?

A

Intramuscular adrenaline

73
Q

What is the effect of intramuscular adrenaline in anaphylaxis?

A

Reverses peripheral vasodilation and reduces oedema
Alleviates hypotension
Reverses airway obstruction/bronchospasm
Increases force of myocardial contraction
Inhibits mast cell activation

74
Q

Why is adrenaline said to be a time-saver rather than a life-saver in anaphylaxis?

A

Reactivation can re-occur in 20% of patients without re-exposure to the antigen

75
Q

What may be required with adrenaline in anaphylaxis?

A

Multiple doses

76
Q

What is required with adrenaline in anaphylaxis?

A

Proper use of the epipen

77
Q

What is it important to do after treatment with adrenaline in anaphylaxis?

A

Continue to monitor pulse, BP, ECG, and O2 sats

78
Q

What factors are considered in a diagnosis of allergy?

A

Clinical history
Blood tests
Skin prick tests
Challenge tests

79
Q

What clinical history is considered in allergy?

A

Atopy
Allergens
Seasonalities
Route of exposure

80
Q

What blood tests are done in diagnosis of allergy?

A

Serum allergen-specific IgE

Serum mast cell tryptase, histamine (systemic granulation)

81
Q

What allergens are skin prick tests done for?

A

Range of allergens

82
Q

What is being looked for in skin prick tests?

A

Wheat and flare reaction of >3mm

83
Q

What do skin prick tests need?

A

Trained personnel

84
Q

When is a challenge test done?

A

Food and drug allergy

85
Q

What is the problem with challenge tests?

A

Slight risk of anaphylaxis on highly sensitised patients

86
Q

How is an allergy managed?

A 
Allergen avoidance/elimination
Education
Medic alert information 
Drugs
Allergen desensitisation
87
Q

How can allergens be avoided/eliminated?

A

Read food levels
House dust mite avoidance
Avoid high risk situations

88
Q

What education is given in management of allergy?

A

Parents to recognise symptoms
Patients to use epipen
Call emegency devices when epipen is used
Schools and social activities

89
Q

What drugs can be given in the management of allergy?

A

Antihistamines
Corticosteroids
Anti-IgE IgG
Anaphylaxis

90
Q

What should be given in antihistamine prevention?

A

Alternating sedating/non-sedating forms

91
Q

How can corticosteroids be administered in allergy management?

A

Topical

Systemic

92
Q

Give an example of an anti-IgE IgG drug

A

Omalizumab

93
Q

What does allergen desensitisation involve?

A

Administration of increasing doses of allergen extracts over a period of years

94
Q

When is allergen desensitisation used?

A

In patients with high risk of systemic attack

95
Q

Under what conditions must allergen desensitisation take place?

A

In a specialist hospital based unit with resuscitation equipment

[ ESA 3- Infection and Immunity (15 decks)

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