Allergy + Hypersensitivity Flashcards

1
Q

What is hypersensitivity?

A

State of altered reactivity in which the body reacts with an exaggerated immune response to foreign antigen

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2
Q

What type of reaction is type I?

A

IgE mediated

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3
Q

What type of reaction is type II?

A

Non-IgE mediated
(Cytotoxic)

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4
Q

What type of reaction is type III?

A

Non-IgE mediated
(Immune complex)

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5
Q

What type of reaction is type IIII?

A

Non-IgE mediated
(Cell mediated)

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6
Q

Describe type I

A

Most common
Allergen
Mild - life threatening

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7
Q

What are some types of allergens?

A

Inhaled materials - eg. pollen
Injected materials - eg. drugs/vaccines
Ingested materials - eg. food
Contacted materials - eg. plant leaves

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8
Q

What are allergens?

A

Antigens that initate an unwanted IgE-mediated reaction

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9
Q

What is the role of IgE in health?

A

Plays role in protection
Rid body of metazoan parasites

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10
Q

Describe the role of IgE in type I reaction?

A

IgE producing B cells activated during sensitisation (first exposure)
IgE binds to Fc receptor on mast cells or CD63 on basophils
IgE recognises allergen and next exposure binds rapidly and causes
immediate degranulation (elicitation)

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11
Q

What do allergic reactions consist of?

A

Immediate reaction followed by late phase response (hours later)

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12
Q

What is immediate reaction caused by?
Allergy

A

Direct effect of mast cell degranulation

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13
Q

What is late phase response caused by?
Allergy

A

Continuous mediator production

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14
Q

What is an example of type I reaction?

A

Atopic eczema

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15
Q

What does atopic mean?

A

Genetic predisposition

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16
Q

Describe eczema

A

Early years
Wide range of allergens
Pruritis (itching)

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17
Q

Describe what happens for eczema to take place

A

Allergen has to pass through physical barrier of epidermis

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18
Q

What is the predisposing factor of eczema?

A

Mutations in genes maintaining barrier function

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19
Q

What is systemic anaphylaxis caused by?

A

Allergens that reach blood stream + activate mast cells

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20
Q

What are the 3 potentially fatal reactions in systemic anaphylaxis?

A

Laryngeal oedema = suffocation
Bronchiole constriction = suffocation
Peripheral oedema = hypotension + heart attack

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21
Q

What reaction can penicillin allergy elicit?

A

Type I
Type II

22
Q

What are the allergy tests?

A

Skin prick
Blood test
Patch test
Food challenge

23
Q

Describe the skin pick test

A

Skin pricked with a tiny amount of the suspected allergen
Skin around the prick will become itchy, red and a wheal will appear

24
Q

Describe blood test

A

Specific IgE test
Measures blood IgE antibody levels in response to allergen

25
Describe patch test
Tests if skin reaction is due to contact with specific allergen *Small amount of allergen added to metal discs taped to your skin for 20 minutes and reaction monitored
26
Describe food challenge
Diagnose food allergy Subject given gradually increasing amounts of the suspected food to which they are allergic and their reaction monitored Can only test one food at each appointment Has to be conducted in an ITU setting (danger to patient)
27
What are the treatments for type I?
Avoid allergen Drugs Immunological treatment
28
Describe treatment using drugs for type I
Antihistamines – compete with histamine for receptors Hydrocortisone – block histamine synthesis Cromoglycate – stabilises mast cells and stops histamine release Epinephrine – best immediate treatment for anaphylactic shock
29
Describe the immunological treatment for type I
hyposensitisation – repeat injections of allergen May work by shifting from IgE to IgG production
30
Describe histamine receptor blockers Antihistamines
Inverse agonists Stabilise receptor in inactive conformation Making excessive stimulation with histamine less possible
31
Describe the stimulation of adrenoreceptors Epinephrine
Increases peripheral vascular resistance Improves blood pressure and coronary perfusion Decreases angioedema = bronchodilation Increases intracellular cAMP in mast cells + reduces release of inflammatory mediators
32
Describe type II
Involves activation of complement by IgG or IgM binding to cell surface antigens
33
What is an example of type II?
Haemolytic anemia
34
What is haemolytic anaemia caused by?
Autoimmune haemolytic anaemia Blood group incompatibility Penicillin
35
Describe type III
Mainly IgG responses + their pathogenesis
36
What does type III involve?
Reactions against soluble antigens circulating in serum
37
What does type III result in?
Inflammatory response leading to tissue injury
38
What is the pathology of type III due to?
Antibody-antigen aggregates in tissues
39
What are examples of type III?
Arthus reaction Serum sickness Oral erythema multiforme (EM)
40
What is Arthus reaction caused by?
Intradermal injection/vaccination Ab-antigen (IgG) complexes deposited in tissues
41
What happens in Arthus reaction?
Localised vasculitis response Complement activation + mast cell sensitisation via Fc receptors Activates phagocytes + localised inflammatory response
42
What is serum sickness?
Systemic Arthus reaction = large quantities of injected antigen
43
What are the symptoms of serum sickness?
Vasculitis Rash Fever Joint swelling/pain
44
What is oral erythema multiforme (OEM)?
Crusty blistering of oral mucosa
45
What is oral erythema multiforme (OEM) caused by?
Deposition of IgM in oral mucous membrane
46
What is type IV directed by?
Pro-inflammatory mediators released by antigen specific T cells
47
What are some type IV examples?
Type 1 diabetes Crohn's disease
48
Describe type 1 diabetes with type IV reaction
Pancreatic beta cell antigen Consequence = beta cell destruction
49
Describe Crohn's disease with type IV reaction
Antigens of intestinal microbiota Consequence = regional intestinal inflammation + scarring
50
How is type IV (delayed) caused?
Excessive release of inflammatory mediators
51
When can type IV occur?
In response to chemicals + metal ions
52
What happens in type IV with nickel or chromate?
Metal ions can alter peptide binding to MHC Class II and promote a CD4+ Th1 response Nickel also activates TLR4 directly