lung immunology Flashcards

1
Q

examples of airway respiratory diseases

A

Allergic airway diseases:
Upper airways: allergic rhinitis
Bronchi: asthma
Alveoli: allergic alveolitis

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2
Q

define hypersensitivity

A

Hypersensitivity: exaggerated response, divided to immunological (allergy) and non-immunological reactions

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3
Q

difference between immunological and non-immunological

A

Immunological: can be IgE-mediated (atopic diseases e.g. Hayfever, eczema and asthma) and non-IgE-mediated (allergic e.g. Farmer’s lung)
Non-immunological: can be intolerance, enzyme deficiency, or pharmalogical (e.g. Aspirin hypersensitivity)

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4
Q

what is allergy?

A

exaggerated immunological response to a foreign substance (allergen) which is either inhaled, swallowed, injected, or comes in contact with the skin or eye; MECHANISM not a disease

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5
Q

Asthmatic airways: have a lot of ?

A

Asthmatic airways: have a lot of IL4/5 and eosinophils

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6
Q

Pathophysiology of seasonal allergic rhinitis:

A

Infiltration of allergens through nasal mucosa
Dendritic cells capture allergens and travel to lymph nodes
B-cells differentiate to IgE producing plasma cells
IgE priming of mast cells

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7
Q

Atopy is?

A

hereditary predisposition to produce IgE antibodies to common allergens; atopic diseases = allergic rhinitis, asthma and atopic eczema; allergic tissue reactions are characterised by infiltration of TH2 cells and eosinophils

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8
Q

what is the allergic march?

A

it describes the common progression of atopic diseases from atopic dermatitis to allergic asthma

eg food allergies from birth but need chronic (several seasons) exposure to develop allergic rhinitis

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9
Q

describe Rhino-conjunctivitis

A

summer hay fever

seasonal/perennial affecting up to 25% of the population; seasonal form affects 10-12% children

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10
Q

Common causes of perennial allergic rhinitis

A

Common causes of perennial allergic rhinitis: house dust mites, cats, dogs, alternaria, cockroaches and horses

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11
Q

Asthma- what does it’s phenotype depend on?

A

Asthma: affects 8-12% population; very heterogeneous, with phenotypes based on control and severity or endotypes (neutrophilic/allergic/eosinophilic/exercise induced)

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12
Q

mechanisms on extrinsic alveolitis

A

Exposure to small allergenic particles that penetrate distal airways (less that 5 microns), captured by antibodies in the interstitium (on pulmonary capillary) causing immunological cascades, complement and neutrophils/macrophages

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13
Q

the principles of treatment of allergic diseases

A

Principles of treating allergic disease: allergen avoidance, anti-allergic medication (antihistamine then intra-nasal steroids) and immunotherapy (desen/hyposensitisation)

Seasonal allergic rhinitis: runny nose, sneezing, congestion, leading to decreased productivity

Allergen immunotherapy: either subcutaneously or daily sublingually to gradually expose to and then desensitise them to allergens; effective and long-lasting although risk of severe reaction, time consuming and standardisation problems

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14
Q

allergen can be either?

A

subcutaneous or sublingual

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15
Q

pros and cons of allergen-injection immunotheraphy (hyposensitisation/ desensitisation)

A

advantages:
effective, produces long lasting immunity

disadvantages:
occasional severe allergic reaction, time consuming, standardisation problems

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16
Q

mechanism on allergic rhinitis

A

Allergic rhinitis:
Allergens pass over epithelium in the airways and are captured by dendritic cells
Dendritic cells migrate to lymph nodes and stimulate TH cells to differentiate to TfH (using IL4) and TH2 cells (using IL9) that activate B-cells and mast cells respectively
TfH cells stimulate B-cells to become plasma cells that secrete allergen specific IgE antibodies that bind to FcE receptors on mast cells
When the allergen cross links IgE antibodies on mast cells, degranulation occurs leading to histamine release

17
Q

mechanism on extrinsic allergic alveolitis

A

Extrinsic allergic alveolitis:
Small allergenic particles penetrate distal airways ant enter alveoli, then interstitium
Particles are captured by antibodies in the interstitium to form antigen-antibody complexes
Complement and immunological cascades are triggered and lymphocytes are recruited

18
Q

Immunotherapy mechanism:

A

subcutaneous/sublingual exposure to traces of the allergen leads to desensitisation because TH cells become Tregs that inhibit TfH cells, stopping the producting of IgE antibodies; they can also cause B-cells to become Bregs that inhibit B-cells or become plasma cells that produce IgG/A antibodies that compete for allergen binding with IgE, reducing the hypersensitivity response