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Module 204 MSK & Immune system > T1 L17 and 18 Atopy, allergy and DTH > Flashcards

T1 L17 and 18 Atopy, allergy and DTH Flashcards

1
Q

What is an allergen?

A

Substance to which IgE antibodies may be produced

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2
Q

What are the steps of the early phase reaction?

A

1) Specific antigen binds to IgE
2) Cross-linking of IgE antibodys by allergen causes clustering of FceR1 receptors
3) Intracellular portion of receptor becomes phosphorylated
4) Resulting intracellular cascade leads to cellular activation
5) Mast cell degranulates releasing histamine, tryptase and other pre-formed mediators

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3
Q

Describe the effects of mast cell activation and granule release on the GI tract

A

Increased fluid secretion
Increased peristalsis

Leading to:
Expulsion of gastrointestinal contents (diarrhoea, vomiting)

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4
Q

Describe the effects of mast cell activation and granule release on the airways

A

Decreased diameter
Increased mucus secretion

Leading to:
Congestion and blockage of airways (wheezing, coughing, phlegm)
Swelling and mucus secretion in nasal passages

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5
Q

Describe the effects of mast cell activation and granule release on blood vessels

A

Increased blood flow
Increased permeability

Leading to:
Increased fluid in tissues causing increased flow of lymph to lymph nodes
Increased cells and proteins in tissues
Increased effector response in tissues

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6
Q

Give examples of allergen sources

A

Pollens
House dust mite faeces
Stinging insect venom

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7
Q

What are the general characteristics of allergens?

A

Proteins
Physical properties that favour transition across mucus membranes
Biologically active, often enzymes
Have moderate homology with self-proteins

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8
Q

What is anaphylaxis?

A

Generalised allergic reaction

Systemic release of histamine leads to generalised vasodilation and fluid loss from circulation to tissues

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9
Q

What are some common triggers for anaphylaxis?

A

Food
Drugs
Insect venom

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10
Q

What are the cardinal features of anaphylaxis?

A 
Typical symptoms
Multi-system
Dramatic
Rapidly follows exposure to antigen
Tends to improve fairly quickly
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11
Q

What is oral allergy syndrome?

A

Most common type of food allergy across UK adults
IgE directed against pollen proteins cross-reacts with homologous proteins in plant-derived food
Exposure to raw fruits, nuts and vegetables causes oral itching

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12
Q

What is rhinitis?

A

Blockage due to type 1 allergy

Sneezing and rhinorrhoea

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13
Q

What is lower airway obstruction?

A

Wheeze due to type 1 allergy

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14
Q

What are examples of seasonal allergens?

A

Pollens

Moulds

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15
Q

What are examples of episodic allergens?

A

Occupational

Animal dander

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16
Q

Why is tolerance required?

A

To prevent autoimmune and inflammatory diseases

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17
Q

What is allergic / atopic march?

A

Progression of disease observed from infancy
Eczema –> food allergy –> rhinitis –> asthma
Allergic disease can present de novo in adults

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18
Q

What would asthma show on biopsy?

A

Inflammatory infiltrate and airway changes known as re-modelling
Thickened basement membrane
Smooth muscle hyperplasia

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19
Q

What does IL-4 lead to?

A

Mucus hypersecretion

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20
Q

What does IL-13 lead to?

A

Bronchial hyper-responsiveness

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21
Q

What does IL-5 lead to?

A

Eosinophil recruitment

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22
Q

What does IL-9 lead to?

A

Mast cell recruitment

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23
Q

What is the late phase allergic reaction?

A

Occurs hours after early phase reaction

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24
Q

What would be shown in a biopsy of late phase allergic reaction?

A

Infiltration with inflammatory cells:
CD4 T-cells
Eosinophils
Mast cells

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25
Q

What is the evidence that Th2 responses are important in allergy?

A

IL-4 required for B-cell class switching to IgE
IL-4 and IL-13 promote mucus hypersecretion
IL-5 required for eosinophil survival
IL-9 recruits mast cells

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26
Q

Describe the genetics of asthma

A

Childhood allergy strongly predicted by presence of allergy in parents
Numerous genetic risk factors identified, none particularly compelling
Allergy epidemic occurred too quickly to be entirely explained by genetics

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27
Q

Describe the hygiene hypothesis

A

Strachan 1989
Low hygiene levels, high pathogen load and helminth infections proposed for skew immunity from Th2 to Th1 and induce regulatory T-cells
High hygiene levels, low pathogen load and absence of helminth infection proposed for skew immunity towards Th2 and reduce production of regulatory T-cells

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28
Q

What factors contribute to developing countries having less allergies?

A 
Large family size
Rural homes, livestock
Intestinal microflora are variable and transient
Low antibiotic use
High helminth burden
Poor sanitation, high orofaecal burden
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29
Q

What factors contribute to westernised countries having more allergies?

A 
Small family size
Affluent urban homes
Intestinal microflora are stable
High antibiotic use
Low or absent helminth burden
Good sanitation, low orofaecal burden
30
Q

What did the LEAP study look at?

A

Is exposure to peanuts protective?
High risk infants recruited and tested for peanut allergy at baseline
After 6 months of age they were randomised to either peanut avoidance or regular consumption and followed to 5 years

31
Q

What were the results of the LEAP study?

A

Those exposed had peanut in the gut
Those not been exposed may be exposed to peanuts through the skin in future. If they already have asthma and skin is already inflammed, then allergen gets presented in an inflammatory context.

32
Q

What is in vivo skin testing?

A

Allergen extract applied as drops
Top layers of epidermis are punctured with lancet
Positive result if wheal and flare occurs within 15 minutes
Results need interpretation in clinical context

33
Q

What is in vitro testing?

A

ELISA

34
Q

Give the 4 main steps of the ELISA

A

1) Plastics coated with purified allergen of interest
2) Incubate with patient serum
3) IgE antibodies in sera of sensitised patient bind to allergens
4) Immobilised IgE antibodies detected with polyclonal anti-IgE detection antibody

35
Q

Give examples of allergy treatments that only resolve symptoms

A

Nasal decongestants e.g. oxymetazoline
Beta2 agonists e.g. salbutamol
Epinephrine

36
Q

What is the mechanism of oxymetazoline?

A

Acts on alpha1 adrenoreceptors causing vasoconstriction

37
Q

What is the mechanism of salbutamol?

A

Acts on beta 2 adrenoreceptors in lung causing smooth muscle relaxation

38
Q

What type of drugs act on early phase mediators?

A

H1 antihistamines
Leukotriene receptor antagonists
Mast-cell stabilisers

39
Q

Give an example of a H1 antihistamine

A

Chlorpheniramine - 1st generation

cetirizine, loratadine, desloratadine, fexofenadine

40
Q

Why can 1st generation antihistamines only be given in hospital?

A

High risk of sedation and drug interactions

41
Q

Give an example of a leukotriene receptor antagonist

A

Montelukast

42
Q

Give an example of a mast-cell stabiliser

A

Sodium cromoglicate

43
Q

Describe the mechanism of corticosteroids

A

1) Steroid receptors found in cytoplasm are complexed with heat-shock protein Hsp90
2) Steroids cross cell membrane and bind to steroid receptor complex which releases Hsp90
3) Steroid receptor complex crosses nuclear mechanism
4) In nucleus, steroid receptor binds to specific gene regulatory sequences which activates transcription.

44
Q

Give examples of inhaled corticosteroids

A

Beclomethasone

Fluticasone

45
Q

Give examples of nasal corticosteroids

A

Beclomethasone
Mometasone
Fluticasone

46
Q

What is omalizumab?

A

Monoclonal antibody directed against IgE

47
Q

How does omalizumab word?

A

Binds to free IgE decreasing cell-bound IgE
Decreases expression of high-affinity receptors
Decreases mediator release
Decreases allergic inflammation, prevents exacerbation of asthma and reduces symptoms

48
Q

What is allergen-specific immunotherapy?

A

Large doses of allergen are administered y subcutaneous injection or sublingually which produces multiple immunological effects

49
Q

What immunological effects occur in allergen-specific immunotherapy?

A 
Induce regulatory T-cell responses to allergens
Reduced Th2 responses
Induced allergen-specific IgG antibodies
Reduction in mast cell responsiveness
Reduce allergen-specific IgE levels
50
Q

What is contact dermatitis

A

Type IV hypersensitivity reaction

51
Q

Describe the process of sensitisation in CD

A

Sensitising agents penetrate skin and react with self-proteins to create protein-happen complexes. These are picked up by Langerhans cells and migrate to regional lymph nodes
Langerhans cells process and present antigens with MHC II
Activated T-cells then migrate to dermis

52
Q

What is a hapten?

A

Small molecule which can’t produce an immune response by itself but can bind to a protein to alter its immunogenicity

53
Q

Describe the process of elicitation in CD

A

Chemokines recruit macrophages
Th1 cells secrete IFN-gamma which increases expression of vascular adhesion molecules and activates macrophages.
TNF-alpha/beta causes local inflammation

54
Q

What is pentadecatechol?

A

Poison ivy lipid that may cross skin and modify intracellular proteins

55
Q

What is patch testing?

A

Done for contact dermatitis
Antigen-impregnated patch placed on back and results read after 2 days.
Examples include nickel, chrome, cobalt, expose resin, lanolin.

56
Q

What is the difference between the clinical features of type I and type IV allergy?

A

Type I has various features consistent with mast cell degranulation
Type IV is an eczematous skin reaction

57
Q

What is the difference between the temporal aspect of type I and type IV allergy?

A

Type I closely follows exposure then improves rapidly

Type 2 has a delay between exposure and symptoms

58
Q

What is the difference between the causative agents of type I and type IV allergy?

A

Type I is almost always a naturally occurring protein or closely related to one
Type IV is various, often synthetic molecules

59
Q

What is the difference between the effector mechanism of type I and type IV allergy?

A

Type I has specific IgE, mast cell degranulation

Type IV has antigen-specific effector Th1 cells

60
Q

How is type I and type IV allergy assessed?

A

Type 1 in allergy clinic. History, skin prick testing, serology for antigen-specific IgE
Type IV in dermatology clinic or allergy clinic. History or patch testing.

61
Q

How are type I and type IV allergy managed?

A

Type I is avoidance, pharmacotherapy and immunotherapy

Typve IV is avoidance

62
Q

When should a skin-prick test be done?

A

History suggestive of IgE mediated allergy

63
Q

What is the test format of skin-prick testing?

A

Allergen extract drops applied to skin, skin punctured. Read after 15min

64
Q

What is a positive result of the skin prick testing?

A

Wheal and flare response

65
Q

When should a patch test be done?

A

History suggestive of contact dermatitis

66
Q

What is the test format of patch testing?

A

Test antigen applied under occlusive dressing. Read after 48h.

67
Q

What is a tuberculin skin test used for?

A

To determine exposure to TB

68
Q

What is tuberculin?

A

Complex mixture of antigens derived from MTB which is injected intradermally in the TST.

69
Q

Why is the tuberculin skin test a poor test for active TB?

A

TB is unlikely to be in the skin so the test will be negative

70
Q

What is the mechanism of the tuberculin skin test?

A

1) Antigen injected into subcutaneous tissue and processed by local antigen presenting cells
2) Th1 effector cell recognises antigen and releases cytokines which act on vascular endothelium
3) Recruitment of phagocytes and plasma to site of antigen injection causes visible lesion

71
Q

What are there results of IGRA test if there is no previous TB exposure?

A

No primed effector memory T-cells specific for MTB

No interferon gamma produced in such a short timeframe

72
Q

What are the results of IGRA test if there is previous TB exposure?

A

Effector memory Th1 cells recognise antigen

Secondary immune response means cytokines are released within short timeframe.

Module 204 MSK & Immune system (44 decks)

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