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Respiratory Diseases & Dermatology > PT4: Inflammation & Allergy in Asthma > Flashcards

PT4: Inflammation & Allergy in Asthma Flashcards

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Dermatology Board Prep flashcards
1
Q

what is extrinsic asthma

A

atopic (allergic), young onset, hyperresponsive

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2
Q

what is intrinsic asthma

A

non-atopic (non-allergic), middle aged, hyperresponsive, more severe airflow limitation

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3
Q

what is allergy

A

changed reacticvity
usually used interchangably with immediate hypersensitivity (involves IgE mediated mast cell degeneration, synonymous with ‘atopy’ or ‘atopic diseases’)

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4
Q

what is atopy

A

allergy

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5
Q

what are allergens

A

antigens that elicit an allergic response

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6
Q

what is anaphylaxis

A

acute severe allergic reaction resulting in respiratory collapse

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7
Q

how is an allergy developed

A

strong genetic influence, allergenic potential, driven by T-helper lymphocyte subset and their products

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8
Q

what Th1 cytokines are involved in allergy

A

interferon-gamma

IL-12

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9
Q

what Th2 cytokines are involved in allergy

A

interleukin IL-4 and IL-3 (overlapping receptor usage with very similar actions)
IL-5, IL-9

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10
Q

what factors favour the Th1 phenotype

A

presence of older siblings, early exposure to day care, TB/measles/hep A infection, rural environment

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11
Q

what type of immunity does a Th1 phenotype give

A

protective immunity

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12
Q

what factors favour the Th2 phenotype

A

widespread use of antibiotics, western lifestyle, urban environment, diet, sensitisation to house-dust mites and cockroaches

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13
Q

what is the T-cell direction of allergic response

A

IL-4 and IL-13 switch B lymphocytes to make IgE antibody

IgE fixes onto FceR on the surface of tissue mast cells

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14
Q

what is IgE

A

relatively rare immunoglobulin in plasma

E= erythematous antibody

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15
Q

how is the IgE antibody used

A

Fc region binds with high affinity to FceR1 on mast cells and basophils
cross linking IgE (by antigen) bound to FceR1 on mast cell surface causes degranulation

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16
Q

what is the times course to develop allergy

A

initial sensitisation may take years; no or very limited symptoms during initial sensitisation and mast cell priming; sensitisation increases over years and re-exposure can trigger mast cell release

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17
Q

what are some examples of mast cell products

A

granule products (histamine)
TNF & other cytokines (inflammation and tissue growth)
proteases (tissue remodelling)
heparins (protective role)
membrane-derived lipid mediators of inflammation (leukotrines, prostanoids)

18
Q

what level of histamine is found in the lungs

A

low level

19
Q

what level of histamine is found in the skin

A

high level

20
Q

what are some examples of H1 receptor antagonists

A

chlorpheniramine, astemizolem cetirizine

21
Q

what are the uses of H1 receptor antagonists

(chlorpheniramine, astemizole, cetirizine)`

A

effective in allergic rhinitus, urticaria
no or little indication in asthma
astemizole and cetirizine have low lipophilicity and less CNS effect

22
Q

what are cromones

A 
disodium cromoglycate (DSCG), nedocromil
mast cell stabalisers that inhibit mediator release from lung mast cells
23
Q

when are cromones effective

A

effective in about half patients
effective against early and late phase asthma; antigen, irritant and exercise induced asthma; prolonged prophylaxis required

24
Q

what are the other actions of cromones

A

inhibit eosinophil chemotaxis

inhibit sensory nerve fibre excitation and neural reflex

25
Q

what is an example of an anti-IgE antibody

A

omalizumab

26
Q

what is the anti-IgE antibody (omalizumab)

A

monoclonal antibody
binds Fc portion of IgE
prevents IgE binding to mast cells
protein drug (must be administered parenterally and very expensive)
approved for IgE mediated severe allergic asthma that is not responsive to glucocorticoids

27
Q

how is immunotherapy used

A

escalating dose antigen under medical supervision, lisenced for use in allergy (not routine asthma), expensive
used for grass and pollen extracts, bee and wasp venom

28
Q

what are the inflammatory mediators in asthma

A

smooth muscle, epithelium, bronchial venules, leukocyte chemotaxis and activation

29
Q

what are some anti-inflammatory drugs used in asthma

A

glucocorticoids, mediator antagonists/inhibitors, cytokine inhibitors/antagonists

30
Q

what are two examples of glucocorticoids

A

prednisolone, budesonide

31
Q

how do glucocorticoids work

A

act mainly via regulating gene transcription (inhibit cytokine transcription, inhibit inflammatory leukocyte migration)
indirectly inhibit phospholipase A2 activity

32
Q

what are mediator antagonists/inhibitors

A

orally active
leukotrine receptor antagonists
leukotrine synthesis inhibitors

33
Q

what does LTRA stand for

A

leukotrine receptor antagonists

34
Q

what are some examples of leukotrine receptor antagonists

A

montelukast, zafirlukast

35
Q

what is an example of leukotrine synthesis inhibitors

A

zileuton

36
Q

what leukotrines are active in asthma

A

LTC4 and LTD4 (cysteinyl leukotrienes); LTB4

37
Q

what are the functions of LTC4 and LTD4 leukotrienes

A

potent constriction of airway smooth muscle, increase vascular permeability (oedema)

38
Q

what is the function of the LTB4 leukoteiene

A

no direct bronchoconstriction, chemotactic for leukocytes

39
Q

what is IL-5

A

growth factor, ‘primes’ and activates, chemotactic

40
Q

what is non-allergic (intrinsic) asthma

A

many asthmatics not allergic, skin test negative (serum IgE levels still elevated), similar symptoms and tissue remodelling, innate immune system involvement

Respiratory Diseases & Dermatology (34 decks)

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