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Year 2 clinical pathology > Week 4 allergy > Flashcards

Week 4 allergy Flashcards

1
Q

What is the definition of Allergy & Hypersensitivity?

A

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

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2
Q

Which hypersensitivity reactions are Ab mediated and which are cell mediated?

A

Types 1-3 = Ab mediated Type 4 = Cell mediated

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3
Q

What type of antibody and antigen causes type 1 hypersensitivity?

A

Ige

Exogenous

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4
Q

What is the response time and appearance of type 1 hypersensitivity?

A

15- 30 minutes reponse time

Appearance –> weal and flare

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5
Q

what is the histology of type 1 hypersensitivity? How is it transfered?

A

basophils & eosinophil

Antibodies is by how it gets transfered

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6
Q

What is another name for type 2 hypersensitivity?

A

cytotoxic

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7
Q

what is another name for type 3 hypersensitivity?

A

immune complex

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8
Q

What is the Immunopathogenesis of type 2?

A

IgM/IgG Ab response against combined self/foreign Ag at the cell surface 2) When Ab binds to Ag on solid surface get complement activation and activation of phagocytic cells, ADCC (Ab dependent cellular cytotoxicity
Cause cell damage

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9
Q

What are the clinical features of type 2? Include the histology invovled in type 2

A

Onset minutes to hours
Cell lysis and necrosis
The histology –> antibody and
complement

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10
Q

What is a common antigen that causes type 2?

A

Penicillin

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11
Q

What are associated diseases with type 2 hypersensitivity?

A

Erythroblastosis fetalis,

Goodpasture’s nephritis

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12
Q

What is Rhesus?

A

Rhesus (Rh) factor is an inherited protein found on the surface of red blood cells. If your blood has the protein, you’re Rh positive. If your blood lacks the protein, you’re Rh negative.

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13
Q

What is the immunopathalogy of type 3?

A

IgG/IgM Ab against soluble antigen- immune complex deposition

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14
Q

Clinical features of type 3?

A

Onset 3-8h
Vasculitis
Histology –> complement and
neutrophils

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15
Q

How is type 1,2,3 trasnfered?

A

Antibody

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16
Q

What sickness does type 3 hypersensitivity cause?

A

Traditional cause-serum sickness

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17
Q

What is the assoicted disease with type 3?

A

SLE

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18
Q

In type 3 hypersensitivity if the antigen entered the body via IV what would be the resulting disease and the site of immune complex deposition?

A

Diseases 1) Vasculitis 2) Nephritis 3) Arthritis Site of deposition
1) Blood vessel walls 2) Renal glomeruli 3) Joint spaces

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19
Q

In type 3 hypersensitivity if the antigen entered the body via subcutaneous route what would be the resulting disease and the site of immune complex deposition?

A

Disease - Arthus reaction

Site - Perivascular area

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20
Q

In type 3 hypersensitivity if the antigen entered the body via inhalation what would be the resulting disease and the site of immune complex

A

Disease - Farmer’s lung Site - Alveolar/Capillary interface

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21
Q

What is the difference beteen type 2 and type 3 in the interaction between antigens and antibodies?

A

Type 2 - Ab against Ag attached to a cell surface so cell lysis
Type 3 - Ab against soluble Ag so immune complex deposition

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22
Q

What is the immunopathalogy of type 4?

A

Antigen specific T-cell mediated cytotoxicity

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23
Q

what is the clinical features of type 4?

A

Delayed onset 48-72h

Apearance Erythema induration

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24
Q

What is Erythema?

A

It is superficial reddening of the skin, usually in patches, as a result of injury or irritation causing dilatation of the blood capillaries.

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25
Q

Common antigen of type 4?

A

Metals-e.g nickel –> cheap metals

Tuberculin reaction

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26
Q

What is Tuberculin reaction?

A

Tuberculin is an extract of Mycobacterium tuberculosis that is used in skin testing in animals and humans to identify a tuberculosis infection

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27
Q

Assoicated disease with type 4?

A

Contact dermatitis

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28
Q

What is the process that causes type 1 hypersensitivity?

A

1) Barrier dysfunction - allowing entry of Ag
2) Sensitisation
3) Changes in T cell sub-sets dominated by Th2
4) IgE Ab produced
5) Allergic symptoms

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29
Q

What contributes to a person developing allergic disease?

A

The lack of infectious drive is a contributory factor in allergic disease

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30
Q

What are the 6 common organs invovled in allergic reaction.

Give example for each of the organs of allergic reaction

A

1) Eyes - allergic conjunctivitis
2) Nose - allergic rhinitis
3) Mouth - oral allergy syndrome
4) Airways - allergic asthma
5) Skin - atopic dermatitis
6) GI tract - food allergy

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31
Q

Why 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

32
Q

What is the immune response to parasitic disease?

A

Increased levels of IgE
Total
Specific to pathogen – cross-reactive

Tissue inflammation with:
eosinophilia & mastocytosis
Basophil infiltration

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

33
Q

What disease are TH1 and TH2 invovled in?

A

TH1 –> management of infection

Th2 –> management of allergic disease

34
Q

Can genetic influences alone cause hypersensitivity?

A

NOT sufficient for disease

ONLY susceptibility, environment required

35
Q

Can you have a hypersensitized reaction on your first time encountering the antigen?

A

No because you can only have a hypersensitive reaction on re-exposure to an allergen to which you have previously been exposed ie. sensitised

36
Q

What are allergens?

A

Allergens are Antigens that initiate an IgE mediated response

37
Q

What is the action of the different TH cells?

A

TH1 –> fight infection
Th2 –> allergy response
Th17 –> fights infection
Treg –> calm down the pathway and block the others

38
Q

What cytokine does TH2 produce to get B cells to produe IgE?

A

IL-4

39
Q

What does production of IL-4 by TH2 do?

A

It signalls to B cells to produce IgE

40
Q

What is the process of type 1 allergic response?

A

1) Exposure to Ag which is presented to T cells by APCs 2) T cell cytokine release resulting in Th2 delineation and B cell activation to produce IgE
3) IgE Fc portion binds to mast cell IgE receptors
4) On re-exposure allergen binds to Fab portion of mast cell bound IgE
5) Cross linking causes release of mediators from mast cells and basophils leading to symptoms

41
Q

What 6 organs are affected in type 1 allergic response?

A 
Smooth muscles
blood vessels
mucous gland 
platelet 
sensory nerve endings 
eosinophil
42
Q

What is the Immunopathogenesis of IgE mediated allergic response?

A

IgE Ab mediated mast cell and basophil degranulation- release of preformed and de novo synthesized inflammatory mediators

43
Q

What is the clinical features of IgE mediated allergic response?

A 
Fast onset (15-30 min)
Wheal and flare
44
Q

Whats invovled in the late phase response to IgE mediated allergic response?

A

Eosinophils

Central role for Th2 T cell

45
Q

What is the pathway of the late phase reaction in IgE mediated allergic response?

A

Arachidonic acid pathway –> produce leukotrienes and/or prostaglandin

46
Q

What process is invovled in the initial phase reaction of IgE mediated allergic response?

A

Degranulation –> Granule contents are realeased including histamine

47
Q

What is the role of Th2 in allergic response?

A

Multiple cytokine release:

Innate inflammatory
Response

Drive for immunoglobulin
production

48
Q

What are the symptoms of RHINITIS?

A

Blocked nose, runny nose - often with eye symptoms

49
Q

What can cause rhinitis?

A

House dust mite, animal danders, pollens

50
Q

What is the treatment for rhinitis?

A

Antihistamines ( deal with immediate response) & Nasal steroids ( deal with long term symptoms)

51
Q

What diseases are in the atopic triad?

A

Asthma, Rhinitis, Eczema

52
Q

What type of hypersensitivity is each of the atopic traid diseases?

A

Asthma - Type 1 hypersensitivity
Rhinitis - Type 1 and 3 hypersensitivity
Eczema - Type 4 hypersensitivity

53
Q

What is the two types of rhinitis? What is the frequency of rhinitis?

A

ALLERGIC or NON-ALLERGIC

Can be perennial or seasonal

54
Q

What is asthma?

A

Disease of INFLAMMATION & HYPER-REACTIVITY of small airways

55
Q

In children what triggers asthma?

A

In childhood - AERO-ALLERGIC stimuli - HOUSE DUST MITE key pathogenic importance

56
Q

What mediates asthma symptoms?

A

IMMEDIATE symptoms are IgE-mediated

57
Q

What process in asthma damages the airways?

A

DAMAGE TO AIRWAYS due to LATE PHASE RESPONSE

58
Q

What is the consequence of damaged airways?

A

DAMAGED AIRWAYS ARE HYPER-REACTIVE to non-allergic stimuli e.g. fumes

59
Q

What two substances produced by mast cells in late phase response is key in ashtma?

A

Leukotrienes and Prostaglandins

60
Q

what are the different types of dermatitis?

A

1) Atopic - eczema 2) Allergic - type 4 hypersensitivity 3) Non-allergic

61
Q

How does dermatitis present clinically?

A

Intense itching, blistering/weeping, cracking of skin

62
Q

What is thought to be a major cause of atopic dermatitis?

A

HOUSE DUST MITE

63
Q

What is treatment for atopic dermatitis?

A

Topical Steroids & Moisturisers

64
Q

What is the process in atopic dermatitis that makes people want to itch?

A

1) Activated T cells release a cytokine called IL31 - T cell itch mediator 2) Directly causes a scratch which leads to a cycle of barrier disruption and further exposure to hapten

65
Q

What is Anaphylaxis?

A

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

66
Q

What are the different ways of diagnosing allergy?

A 
History
Specific IgE (>0.35 KuA/L)
Skin prick test (>3mm wheal) 
Intra-dermal test
Oral challenge test – Gold standard
Basophil activation test
Component resolved diagnostics
67
Q

What is Basophil Activation Test?

A

Mix patients blood with allergen Upon cross linking basophils upregulate the expression of specific activation markers which can be detected

68
Q

What is the advantage and disadvantage of doing specific IgE test?

A

Adv–> safe
Dis–> False negatives
False positives

69
Q

What is the advantage and disadvantage of doing skin prick test?

A

Adv–> Quick
Patient satisfaction

Dis–> False negatives, alse positives, Antihistamines, Slight risk

70
Q

What are the symptomatic treatment for allergic reaction?

A

Antihistamines, Steroids, Adrenaline

71
Q

What is specific treatment for allergic reaction?

A

Specific – Immunotherapy (Subcutaneous or Sublingual

72
Q

When is specific immunotherapy used to treat allergic reactions?

A

Life threatening reactions to Wasp & Bee sting
Severe Hay fever
Animal dander allergy

73
Q

When is specific immunotherapy not useful in treating allergic reactions?

A

Multiple allergies
Food allergy
Allergic rashes – Eczema, Urticaria

74
Q

What is the general idea of immunotherapy?

A

Trick the immune system to tolerate the antigen through controlled exposure Switch from Th2 to Th1 response W

75
Q

What is the 6 most common food allergies?

A 
COW’S MILK
EGG
LEGUMES - PEANUT; SOYBEAN; TREE NUTS
FISH
CRUSTACEANS / MOLLUSCS
CEREAL GRAINS
76
Q

What is the clinical manifestation of food allergy to the Gastrointestinal,Respiratory , Cutaneous system?

A

Gastrointestinal
vomiting, diarrhoea, oral symptoms

Respiratory (upper & lower)
rhinitis, bronchospasm

Cutaneous
urticaria, angioedema
role of food in atopic dermatitis unclear

Anaphylaxis

77
Q

What are the 4 common clinical manifestations of adverse reactions to food?

A

1) Urticaria 2) Angioedema 3) Bronchospasm 4) Anaphylaxis

Year 2 clinical pathology (21 decks)

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