Allergic Disease Flashcards

1
Q

Hypersensitivity

A

Undesirable, damaging or discomfort producing reactions produced by the normal immune system, directed against inocuous antigens in a pre-sensitised (immune) host

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2
Q

Type II hypersensitivity

A

Cytotoxic

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3
Q

Immunopathogenesis of Type II hypersensitivity

A

IgG/IgM Ab response against combined self/foreign antigen at the cell surface-complement activation/phagocytosis.

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4
Q

Clinical features for type II hypersensitivity

A

Mins to hours. Cell lysis and necrosis.

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5
Q

Common antigen for type II hypersensitivity

A

Penicillin

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6
Q

Associated diseases with type II hypersensitivity

A

erythroblastosis fetalis, goodpasture’s nephritis. Rh reaction with mother/foetus.

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7
Q

Type III hypersensitivity reaction

A

Immune complex

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8
Q

Immunopathology of type III hypersensitivity reaction

A

IgG/IgM Ab against soluble antigen-immune complex deposition.

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9
Q

Clinical features of type III hypersensitivity

A

Onset 3-8 hours. Vasculitis.

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10
Q

Traditional cause for type III hypersensitivity reaction

A

Serum sickness

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11
Q

Associated diseases for type III hypersensitivity reaction

A

SLE

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12
Q

Type III reaction to IV route of antigen

A

Vasculitis, arthritis, nepthritis

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13
Q

Type III reaction to SC route of antigen

A

Arthus reaction-perivascular area

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14
Q

Type III reaction to inhaled route of antigen

A

Farmer’s lung

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15
Q

Type IV hypersensitivity reaction

A

Delayed- no Ab involved

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16
Q

Immunopathology of type IV hypersensitivity

A

Antigen specific T cell mediated cytotoxicity

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17
Q

Clinical features of type IV hypersensitivity

A

Metals e.g. nickel (tuberculin reaction)

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18
Q

Associated diseases of type IV hypersensitivity

A

Contact dermatitis

19
Q

Immunopathology of type 1-anaphylaxis IgE mediated hypersensitivity

A

Increased IgG levels
Tissue inflammation with eosinophils, mastocytosis, basophil infiltration.
Presence of CD4 cells secreting Il4, Il5, Il13

20
Q

Hygeince hypothesis

A

More exposure to infections, less allergies. Mechanisms is Th1-Th2 deviation (Th1-infection, Th2-allergy)

21
Q

Association between genetics and rhinitis

A

None, as opposed to asthma and atopic dermatitis

22
Q

What happens to the T cell activation in allergic reactions

A

Treg pathway suppressed, Th1 and Th2 pathways are activated.

23
Q

IgE Abs are induced by which cytokines?

A

Il-4

24
Q

Sensitisation

A

B cells activated by Th2 cells-produce IgE Abs, induced by Il-4 cytokines

25
Q

What happens when an allergen is in contact with a pre sensitised host?

A

Antigen binds to fab region of IgE on sensitised mast cell, triggering the release of vasoactive amines.

26
Q

Immunopathogenesis of type I hypersensitivity

A

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

27
Q

Clinical features of tyep I hypersensitivity

A

fast onset (15-30 mins) wheal and flare

28
Q

Late phase response of type I hypersensitivity

A

Eosinophils, central role for Th2 T cell

29
Q

Describe the initial response of the mast cell in type I hypersensitivity, following antigen binding to IgE on surface of mast cell

A

Degranulation-histamine, proteases, chemotactic factors

30
Q

Describe the late phase reponse of mast cell activation in type I hypersensitivity

A

Cytokines

Arachidonic acid-leukotrienes and prostaglandins

31
Q

3 roles of the Th2 cell

A

Activates B cells-drives Ab production
Activates macrophages-innate inflammatory response
Activates other cells-multiple cytokine release

32
Q

3 parts of the atopic triad and what form of hypersentivity each of them are

A

Rhinitis- 1
Asthma- 1
Atopic dermatitis- 4

33
Q

Is astham in the upper or lower airways?

A

Lower

34
Q

Which cytokine triggers pruritis (scratch)

A

IL-31

35
Q

Anaphylaxis

A

Acute, potentially life threatening, IgE mediated systemic hypersensitivity reaction. 3 types- 3 most severe.

36
Q

Allergic status is given if you have a specific IgE level of what?

A

greater than o.35kua/L

37
Q

What is positive result for the skin prick test?

A

> 3mm wheal

38
Q

Describe the skin prick test

A

-ve control: saline solution (shouldn’t react)
+ve control: histamine (everyone should react)
Pollen/potential antigen

39
Q

Describe the basophil activation test

A

If sensitised, basophils will be activate by antigen -blood test

40
Q

4 types of tests for allergices

A

Skin prick test
Intra-dermal test
Oral challenge
Basophil activation test

41
Q

Mechanisms of immunotherapy

A

Switching pathways from Th2-Th1 or inducing Treg pathway. Modifying T cells to activate B cells to make different antibodies.

42
Q

Describe the skin prick test

A

-ve contcol e.g. saline solution
+ve control e.g. histamine
Potential antigen
+ve result if greater than 3mm wheal

43
Q

Name 4 allergy tests

A

Skin prick test
Intradermal test
Oral challence
Basophil activation test (blood test)

44
Q

Mechanisms of immunotherapy

A

Switching pathways Th2-Th1 or inducing Treg pathway.

Modifying T cells to activate B cells to make different antibodies