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Allergy Flashcards

1
Q

How many types of hypersensitive reactions are there

A 
4 types
Type 1- 3 are antigen mediated.
Type 4 is cell mediated.
Type 1- anaphylaxis
Type 2- cytotoxic
Type 3- immune complex
Type 4- delayed type
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2
Q

What are the stages in developing an allergy

A
  • Exposed to antigen
  • APC and B cells take up antigen and present to T cells.
  • T cells recognise the antigen
  • T cells tell B cells to make the antibody.
  • Re- exposure results in antigen antibody complex forming.
  • B cell- Activate complement and attract phagocytic cells.
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3
Q

Type 2 reaction involve which immunoglobulins

A

IgG/IgM

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4
Q

what is another name for type 2 hypersensitivity

A

cytotoxic

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5
Q

What are the clinical features of type 2 hypersensitivity

A

– Onset minutes to hours

– Cell lysis and necrosis

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6
Q

On what surface must the antigen be to trigger a Type 2 hypersensitivity reaction

A

cell surface.

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7
Q

what is a common allergen for type 2 hypersensitivity

A

penicillin

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8
Q

what 2 conations are associated with type 2 hypersensitivity

A

– Erythroblastosis fetalis,

– Goodpasture’s nephritis

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9
Q

What is another name for typer 3 hypersensitivity

A

immune complex

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10
Q

Type 2 reaction involve which immunoglobulins

A

IgG/IgM

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11
Q

What type of antigen is needed for a type 3 hypersensitivity reaction

A

Soluble.

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12
Q

What are the clinical features of at type 3 hypersensitivity reaction

A

– Onset 3-8h

– Vasculitis- when immunocomplexes are filtered through blood vessels it leads to.

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13
Q

what is the tradition cause of typer 3 hypersensitivity

A

serum sickness- due to serum form other animal used to treat a condition e.g. horse serum in tetanus.

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14
Q

What conditions is type 3 hypersensitivity associated with

A

SLE

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15
Q

What other name is given to type 4 hypersensitivity reactions

A

delayed

no antigen- antibody complex.

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16
Q

What type of cell mediated response is type 4 hypersensitivity

A

– Antigen specific T-cell mediated cytotoxicity

– Antigen is taken up and presented to immune cells which can cause tissue damage.

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17
Q

what are the clinical features of type 4 hypersensitivity

A

– Delayed onset 48-72h
– Erythema induration
➢ Put allergen on skin and then leave for 48-72 hrs to see if the reaction occurs.

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18
Q

What are the common antigens for type 4 hypersensitivity

A

metals e.g. nickel

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19
Q

What condition is associated with type 4 hypersensitivity

A

contact dermatitits.

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20
Q

What is the hygiene hypothesis.

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
  • Change in environment- you get less infection and hence more allergens.
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21
Q

What are Th1 and Th2 used for

A

Th1 -infections

Th2- allergy

22
Q

How are suceptibilty genes involved in sensing the environment.

A

group of genes that encode molecules that directly modulate the effect of environmental risk factors for allergic disease.
e.g – Polymorphisms of glutathione-S-transferase genes have been shown to modulate the effect of exposures involving oxidant stress, such as tobacco smoke and air pollution on asthma susceptibility

23
Q

How are suceptibilty genes involved in barrier function

A

– genes which are responsible for epithelium regulation e.g. ORMDL3/GSDML,34 PCDH1,24 and C11orf30.

24
Q

How are suceptibilty genes involved in the regulation of (atopic) inflammation

A

– This group includes genes that regulate TH1/TH2 differentiation and effector function.
– includes the genes shown to regulate the level of blood eosinophilia

25
How are suceptibilty genes involved in tissues response genes
– includes genes that modulate the consequences of chronic inflammation. – Expressed in fibroblasts and smooth muscel – Some genes affect more than one disease component.
26
Do you get an allergic response on first encounter with a allergen
No | first time you sensitise yourself and then the second time you actually develop a response.
27
How does a allergen cause an allergy
– Defect in the barrier and allergen enters. – Allergen causes damage to the barrier and enter – Allergen taken up and peptides displayed by the dendritic cells – These expose the allergen to T cells (TH2 allergy) – Primary response in up regulation of the allergen.
28
How is Ig E produced
* Th2 cells make cytokines- IL4 | * IL4 drives B cells to make Ig E.
29
what cells do IgE attach to
mast cells.
30
What is the function of mast cells once allege binds to it.
Release histamines protease, and chemotactic factors e.g. ECF, NCF. Secondary de novo molecules such as leukotriene and prostaglandins are made via arachdonic acid.
31
what are the clinical features of Type 1 hypersensitivity
Fast onset (15-30 min)
32
what is the role of Th2
* Multiple cytokine release: IL4 * Innate inflammatory Response by macrophages * Drive for immunoglobulin production by B cells.
33
How is B and T cell memory developed
* Differentiation and clonal expansion of allergen-specific T helper 2 (TH2) cells. * production of cytokines (interleukin-4 (IL-4) and IL-13), which induce immunoglobulin class switching to IgE and clonal expansion of naive and IgE+ memory B-cell populations.
34
what 3 conditions are in the atopic triad
asthma (type 1), rhinitis(type 1 ) and eczema (type 4)
35
where are most cells in asthma and rhinitis
nasal mucosa or airways. | this is were the allergen is exposed.
36
symptoms of rhinitis
• Blocked nose, runny nose - often with eye symptoms
37
most common cause of rhinitis
house dust mite, animal dancers and pollen.
38
what is the treatment for rhinitis
Antihistamines (immediate) & Nasal steroids (chronic)
39
most common cause of asthma
house dust mite.
40
what causes the damage to at the airways
IgE mediated | • DAMAGE TO AIRWAYS due to LATE PHASE RESPONSE- WHICH IS ARACHDONIC ACID MEDIATED.
41
what is the most common cause of atopic dermatitis
house dust mite.
42
symptoms of dermatitis
Intense itching, blistering/weeping, cracking of skin
43
what tests are used to diagnose allergies
• Specific IgE (>0.35 KuA/L) • Skin prick test (>3mm wheal). – Test saline, histamine and potential allergen and then prick the skin were each of these are applied so they can enter the skin. – Should react to histamine and allergen but not saline solution – Can have unusual results due to skin sensiity in people e.g negative test for antigen even though they are allergic because the skin is not sensitive or on antihistamines. – Could have chronic epturia- have allergic reaction to something one time but not another. • Intra-dermal test- similar to SPT but you get more of the substance in the skin • Oral challenge test – Gold standard – Give peanut- see if reaction occurs, if not give more and more over time. • Basophil activation test- test makers which are higher in basophil activation. • Component resolved diagnostics
44
Treatment for allergic reactions
if symptomatic • Antihistamines- early response treatment • Steroids- late/ delayed response tretament • Adrenaline- treat anaphylaxis. Only used is other 3 don't work Immunotherapy (Subcutaneous or Sublingual)- trick immune system into thinking that what they are doing (reacting to the allergen) is wrong.
45
when can immunotherapy be used
* Life threatening reactions to Wasp & Bee sting * Severe Hay fever * Animal dander allergy
46
when is immunotherapy not useful
* Multiple allergies * Food allergy * Allergic rashes – Eczema, Urticaria
47
2 main methods of immunotherapy
1. Direct pathway from Th2 to Th1 | 2. Modify T cells so they produce other antibodies except Ig E.
48
What are the major food allergies
* Water soluble glycoproteins 10 - 60 kd * COW’S MILK * EGG * LEGUMES - PEANUT; SOYBEAN; TREE NUTS * FISH * CRUSTACEANS / MOLLUSCS * CEREAL GRAINS
49
Clinical symptoms caused by food allergies
``` – Gastrointestinal • vomiting, diarrhoea, oral symptoms – Respiratory (upper & lower) • rhinitis, bronchospasm – Cutaneous • urticaria (hives=rash), angioedema (swelling in deep layers of skin) • role of food in atopic dermatitis unclear – Anaphylaxis ```
50
most common drug allergy
IgE mediated penicillin allergy
51
clinical signs of penicillin allergy
angioedema, bronchospasm, anaphylaxis.

Clinical Pathology (45 decks)

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