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S2 Case 3 - asthma & COPD > Allergy + Hypersensitivity > Flashcards

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
Q

Describe patch test

A

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
Q

Describe food challenge

A

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
Q

What are the treatments for type I?

A

Avoid allergen
Drugs
Immunological treatment

28
Q

Describe treatment using drugs for type I

A

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
Q

Describe the immunological treatment for type I

A

hyposensitisation – repeat injections of allergen
May work by shifting from IgE to IgG production

30
Q

Describe histamine receptor blockers
Antihistamines

A

Inverse agonists
Stabilise receptor in inactive conformation
Making excessive stimulation with histamine less possible

31
Q

Describe the stimulation of adrenoreceptors
Epinephrine

A

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
Q

Describe type II

A

Involves activation of complement by IgG or IgM binding to cell surface antigens

33
Q

What is an example of type II?

A

Haemolytic anemia

34
Q

What is haemolytic anaemia caused by?

A

Autoimmune haemolytic anaemia
Blood group incompatibility
Penicillin

35
Q

Describe type III

A

Mainly IgG responses + their pathogenesis

36
Q

What does type III involve?

A

Reactions against soluble antigens circulating in serum

37
Q

What does type III result in?

A

Inflammatory response leading to tissue injury

38
Q

What is the pathology of type III due to?

A

Antibody-antigen aggregates in tissues

39
Q

What are examples of type III?

A

Arthus reaction
Serum sickness
Oral erythema multiforme (EM)

40
Q

What is Arthus reaction caused by?

A

Intradermal injection/vaccination
Ab-antigen (IgG) complexes deposited in tissues

41
Q

What happens in Arthus reaction?

A

Localised vasculitis response
Complement activation + mast cell sensitisation via Fc receptors
Activates phagocytes + localised inflammatory response

42
Q

What is serum sickness?

A

Systemic Arthus reaction = large quantities of injected antigen

43
Q

What are the symptoms of serum sickness?

A

Vasculitis
Rash
Fever
Joint swelling/pain

44
Q

What is oral erythema multiforme (OEM)?

A

Crusty blistering of oral mucosa

45
Q

What is oral erythema multiforme (OEM) caused by?

A

Deposition of IgM in oral mucous membrane

46
Q

What is type IV directed by?

A

Pro-inflammatory mediators released by antigen specific T cells

47
Q

What are some type IV examples?

A

Type 1 diabetes
Crohn’s disease

48
Q

Describe type 1 diabetes with type IV reaction

A

Pancreatic beta cell antigen
Consequence = beta cell destruction

49
Q

Describe Crohn’s disease with type IV reaction

A

Antigens of intestinal microbiota
Consequence = regional intestinal inflammation + scarring

50
Q

How is type IV (delayed) caused?

A

Excessive release of inflammatory mediators

51
Q

When can type IV occur?

A

In response to chemicals + metal ions

52
Q

What happens in type IV with nickel or chromate?

A

Metal ions can alter peptide binding to MHC
Class II and promote a CD4+ Th1 response
Nickel also activates TLR4 directly

S2 Case 3 - asthma & COPD (25 decks)

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