Asthma Flashcards
What is asthma? Give a brief description.
- Chronic, relapsing, inflam’y airway dx characterised by cough, wheeze, SOB and chest tightness.
- Asthma is an obstructive pulmonary disease.
-
Airways demonstrate:
- reversible bronchoconstriction as a result of hyper-reactivity,
- increased mucus production, and
- sm mm hyperplasia.
What are the major types of asthma?
Atopic - most common
Non-atopic
Drug-induced
Occupational
What is atopic asthma? Give a brief summary.
- Type I hypersensitivity reaction
- More common in children
- Family history is common
- Often accompanied by:
- eczema,
- allergic rhinitis (hayfever) and
- allergic conjunctivitis.
- Triggers can be defined by skin testing or RadioAllergoSorbent Test (RAST)
- Common triggers include:
- dust,
- pollens,
- foods,
- roach or animal dander.
What is non-atopic asthma? Give a brief summary.
- Also known as Intrinsic Asthma
- Associated with hyper-irritable airway mucosa
- Often triggered by viral URTI (rhino or parainfluenza virus)
- Viral mucosal irritation decreases the threshold for vagal irritant receptors
- Pollutants also can trigger via inflam’n and hyper-react’y
Describe the pathogenesis of asthma.
- Charcterised by Acute **and **Late Phase reactions.
A trigger (eg environmental irritant) results in TH2 cells:
- secreting cytokines -> allergic inflam’n
- stimulate B cells to produce IgE. IgE binds to epithelial mast cells.
-
Acute Phase
- IgE mediated - > Type 1 hypersensitivity reaction
- IgE coated Mast Cells bind antigen.
- -> release of:
- primary mediators (eg leukotrienes)
- secondary mediators (eg cytokines and neuropeptides)
- -> bronchospasm, oedema, mucus secretion and leukocyte recruitment
- Bronchospasm is triggered by direct stim’n of subepithelial vagal receptors
-
Late Phase
- Mediated by recruited leukocytes (eosinophils and lymphocytes) ->
- persistent bronchospasm
- oedema
- lekocyte infiltration
- loss of damaged epith’l cells
- Major Basic Protein of eosinophils - epithelial damage
- Mediated by recruited leukocytes (eosinophils and lymphocytes) ->
What is airway remodelling in asthma?
Airway remodelling is a response to the repeated inflam’n and allergen exposure seen in asthma. It comprises of structural changes to the epithelial wall of small bronchi. It includes:
- hypertorhy and hyperplasia of bronchial sm. mm
- epithelial inj’y
- Inc’d airway vasc’y
- Inc’d subepithelial mucus gland hyperplasia and hypertrophy
- Deposition of subepithelial collagen
What are some of the complications of asthma? (conditions)
What is not a complication of asthma? *
Complications: Emphysema, chronic bronchitis, bronchiectasis, cor pulmonale
Not complications: Amyloidosis
Name five histological findings in asthma. *
- Hypertrophied sm mm and submucosal mucus glands.
- Thickened basement membrane of bronchial epithelium.
- Oedema and inflam’y infiltrate in bronchial walls.
- Whorls of shed epithelium within mucus plugs (Curshman Spirals).
- Collections of crystalloids made up of eosinophil binding protein (Charcot-Leyden crystals).
What is the cause of the thickened (hypertrophied) sm mm seen in the asthmatic lung? *
Chronic bronchoconstriction.
What are the primary mediators in asthma?
Neutrophilic and eosionophilic chemotactic factors.
What is the most common trigger of intrinsic asthma?
Viral infections.
Which immunologic cells are responsible for the pathogenesis of atopic (extrinsic) asthma?
Beta Cells -> IgE prod’n
Induction of TH2 cells
Growth of mast cells
Activation of eosinophils
Release of IL4 and IL5
