Allergy Flashcards

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1
Q

define hypersensitivity

A

immune response that causes collateral damage to self

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2
Q

what mediates type 1 hypersensitivity reactions

A

IgE

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3
Q

what mediates type 2 hypersensitivity reactions

A

IgG

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4
Q

what mediates type 3 hypersensitivity reactions

A

immune complex mediated

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5
Q

what mediates type 4 hypersensitivity reactions

A

cell mediated (TH1, TC cells)

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6
Q

name 2 other allergic disorders

A

eczema and rhinitis

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7
Q

when does a type 1 allergy occur after exposure to allergen

A

immediate- minutes and up to 2 hours after

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8
Q

what are the routes of contact of allergens

A

skin contact, inhalation, ingestion and injection

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9
Q

describe the pathophysiology of sensitisation to an allergen

A

antigen binds to dendritic cells which then activate T cells (TH2) which produce IL-4, IL-5, IL-13 which activate B cells to create allergen specific IgE which acitvate mast cells to produce histamines, leukotrienes, cytokines, prostaglandins

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10
Q

what is urticaria and its features

A

compressible dermal swelling, very itchy- lesions appear within 1 hour and last 2-6 hours (up to 24hrs)

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11
Q

what is angioedema and its features

A

localised swelling of subcutaneous tissue or mucous membranes-non pitting oedema- not itchy

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12
Q

what happens to respiratory function during an allergic reaction

A

lowered

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13
Q

what is anaphylaxis

A

severe life threatening generalised or systemic hypersensitivity reaction

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14
Q

what are the symptoms of anaphylaxis

A

rapidly developing, pharyngeal or laryngeal oedema, bronchospasm with tachypnoea, hypotension, tachycardia, associated skin and mucosal changes

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15
Q

what investigations can be made into allergies

A

history (most important), specific IgE (RAST- blood test for specific allergen), skin prick or prick prick test, challenge test, serum mast cell tryptase levels (during anaphylaxis)

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16
Q

what is more accurate specific IgE or skin prick test

A

skin prick

17
Q

when do you do a challenge test

A

only if SPT negative

18
Q

how are allergies managed

A

avoidance

1- antihistamines (prevent effects of mast cell activation)
2-corticosteroids (anti-inflammatory agents (oral prednisolone))

adrenaline autoinjector (for anaphlyaxis)

19
Q

what dosage of adrenaline should adults get

A

300 micrograms

20
Q

what dosage of adrenaline should children get

A

150 micrograms

21
Q

how many pens should each patient be perscribed

A

2

22
Q

how other the IgE can hypersensitivity reactions be mediated

A

direct mast cell degranulation (morphine, aspirin, NSAIDs)

metabolic (lactose intolerance)

toxic (scombroid fish toxin)

23
Q

what type of reaction is allergic contact dermatitis

A

type 4, delayed hypersensitivity, (after 24-48hrs)

24
Q

describe the pathophysiology of non IgE reactions

A

Sensitization phase (afferent phase). Haptens penetrate the epidermis (step 1) and are taken up by epidermal cells, including skin.
Dendritic cells (DCs) migrate to the draining lymph nodes (step 2), where they present haptenated peptides to both CD8+ effector T cells
and downregulatory CD4+ T cells (step 3). Specific T-cell precursors clonally expand in draining lymph nodes, recirculate via the blood,
and migrate to tissues, including the skin (step 4). (Right) Elicitation phase (challenge phase, efferent phase). When the same hapten is
applied to the skin, it is taken up by epidermal cells, including skin DCs and keratinocytes (step 5), which present haptenated peptides to
specific T cells. Activation of CD8+ cytotoxic T lymphocytes induces apoptosis of keratinocytes and production of cytokines and
chemokines by skin resident cells (step 6). This leads to the recruitment of leukocytes from the blood to the skin. CD4+ T cells may block
activation/expansion of CD8+ effectors in lymph nodes during sensitization and in the skin during the elicitation phase of contact hypersensitivity

25
Q

what are the sensitisation cells of the skin

A

langerhan cells (dendritic cells)

26
Q

what type of reaction is irritant contact dermatitis

A

non immunological, doesnt reqcuire prior sensitisation, contact with agents that abrade irritate and traumatise the skin

27
Q

name 2 endogenous skin reactions

A

atopic eczema, psoriasis

28
Q

what are the managements for contact dermatitis

A

avoidance, emollients, topical steroids, UV phototherapy, immunosuppresants

29
Q

what mediates type 2 hypersensitivity reactions

A

IgG and IgM antibodies and complement

30
Q

describe the initial sensitisation phase of type 4 delayed reactions

A

dendritic antigen presenting cells langerhans in skin) (antigens binds to MHC-2) migrates to regional lymph nodes, activates Y cells to produce pool of memory T cells in lymph nodes

specific memory T cells released and distributed throughout circulation to encounter antigen in future

31
Q

describe what happens in a type 4 reactions when there is subsequent challenge with antigen

A

antigen on dendritic (langerhan) cell migrates to dermis and encounters and activates specific T cells

release of cytokines from T cells leading to further cell recruitment

32
Q

name 4 types of cutaneous type 4 hypersensitivity

A

allergic contact dermatitis

photo allergy

skin response to bacteria, fungus, viruses

abnormal delayed response in atopic eczema

33
Q

describe contact dermatitis

A

small blisters and erosions due to delayed hypersensitivity to irritant

34
Q

name three types of cutaneous type 1 reactions and what causes them

A

urticaria- red wheals, caused by dilated blood vessels and leakage o fluid into surrounding tissue

angio-oedema- deeper cutaneous reaction than urticaria, causing swelling of sub-cutaneous tissues including mucous membranes

anaphylaxis- w/ urticaria +/- angio-oedema, laryngeal swelling, bronchospasm, hypotension