obstructive airway disease Flashcards
what are obstructive airway diseases?
asthma, chronic bronchitis, emphysema
Describe the airway in patients with COPD.
(alveolar walls, then smooth muscle) large amounts of mucosa crush the lumen.
what is atopic and non-atopic asthma?
atopic = associated with allergens as the main cause of trigger (extrinsic) non-atopic = exercise induced (intrinsic)
what is in the asthma triad?
- reversible airflow obstruction
- airway inflammation
- airway hyperresponsiveness
what is the evolution of asthma?
1- bronchoconstriction - brieft symptoms
2- chronic airway inflammation - exacerbations AHR
3 - airway remodelling - fixed airway obstruction.
what are signs of remodelling in asthma?
- basement membrane thickens
- collagen deposits in the submucosa
- hypertrophy of smooth muscles
Describe the inflammatory cascade in asthma.
inherited or acquired factors; genetic predisposition or viral, allergens or chemicals > eosinophil inflammation > mediators Th2 cytokines > twitchy smooth muscle (hyperreactivity)
how is the inflammatory cascade prevented in asthma?
- avoidance of precipitate
- anti-inflammatory medication; corticosteroids, cromones, theophylline
- antileukotrines or antihistamines monoclonal antibodies; anti-IgE or anti-interleukin-5
- bronchodialators; B2 agonists, muscarinic agonists.
what are the signs of asthma?
- episodic symptoms and signs
- diurinal variability = nocturnal/early morning
- non- productive cough, wheeze
- triggers
- associated atopy increased IgE
- blood eosinophilia greater than 4%
- responsive to steroids or beta agonists
- family history
- wheezing due to turbulent airflow.
how do we diagnose asthma?
- diurinal variation of peak flow
- history and examination
- reduced forced expiratory ratio (FEV1/FVC)
- reversibility to inhaled salbutamol is greater than 15%
- provocation testing - bronchospasm caused by exercise/histamine/ methacholine/ mannitol
Describe COPD
a multicomponent disease process caused by noxious particles or gases e.g. smoking
-mucocillary dysfunction, inflammation and tissue damage leads to development of obstruction and ongoing disease progression
Describe the disease process in COPD
Cigarette smoke and other irritants activate macrophages and airway epithelial cells in the respiratory tract which release neutrophil chemotactic factors, including interleukin 8 (IL-8)and leukotriene B4. Neutrophils and macrophages then release proteases that break down connective tissues in the lung parenchyma and also stimulate mucus hypersecretion. Proteases are normally counteracted by protease inhibitors such as a1-antitrypsin, secretory leukoprotease inhibitor (SLPI) and tissue inhibitors of matrix metalloproteinases.
In COPD there appears to be an imbalance between proteases and antiproteases (either an increase in proteases, or a deficiency of antiproteases) which lead to inflammatory changes in the airways including damage of the respiratory mucosa.
what are characteristic of chronic bronchitis?
- chronic neutrophilic inflammation
- mucus hypersecretion
- mucocilary dysfunction
- altered lung microbiome
- smooth muscle spasm and hypertrophy
- partially reversible
what are characteristics of emphysema?
- alveolar destruction
- impaired gas exchange
- loss of bronchial support
- irreversible
what are the signs of COPD?
-chronic symptoms - non- episodic
-smoking
-non-atopic
-daily productive cough
-progressive breathlessness
-frequent ineffective exacerbations
-chronic bronchitis - wheezing
-emphysema (reduced breath sounds)
-late onset
non-allergic
-no diurnal variability
-neutrophilic inflammation
