Obstructive Airways Disease - Overview Flashcards
describe obstructive airway disease/syndrome
takes place in airways
e.g. asthma, chronic bronchitis, emphysema, ACOS (asthma/COPD overlap syndrome) - smokers with features of both asthma and COPD (COPD with reversibility and eosinophilia who are steroid responsive)
describe asthma
chronic inflammation disease of both large (conducting zone 0-8) and small (acing zone 17-23) airways
eosinophil inflammation
describe COPD
multicomponent disease (nothing to do with Th2 response) process due to noxious particles or gases (smoking)
MUCOCILIARY DYSFUNCTION - hyper secretion of mucous (enlargement of cells and oedema)
TISSUE DAMAGE - obstruction in lumen due to mucous
smooth muscle can go into bronchospasm
alveolar wall can be cut (airway has nothing to support it)
neutrophilic INFLAMMATION
these components are associated with the development of obstruction and ongoing disease process which leads to obstruction of airflow and symptoms of COPD
describe different types of asthma
early/late onset
atopic/non-atopic - allergen in relation to IgE
extrinsic - identifiable extrinsic allergen factor
intrinsic - no identifiable allergen factor
describe the asthma triad
reversible airflow obstruction (spontaneous variability of airways geometry throughout day)
airway inflammation
airway hyper responsiveness (airway becomes excessively twitchy and sensitive)
describe the dynamic evolution of asthma
broncho-constriction - brief symptoms
chronic airway inflammation - exacerbations AHR
airway remodelling - fixed airway obstruction
describe the hallmarks of remodelling in asthma
thickening of basement membrane
collagen deposition of submucosa
hypertrophy of smooth muscle
desquamation of airway epithelium
describe the inflammatory cascade in asthma
inherited or acquired factors; genetic predisposition, viral, allergen or chemical - avoidance of precipitant
eosinophilic inflammation - anti-inflammatory medication;
corticosteroids (attack eosinophils, the only drugs shown to normalise mucosal increase), croons, theophylline
mediators, Th2 cytokines - antileukotrienes or antihistamines, monoclonal antibodies (anti-IgE, anti-IL5)
twitchy smooth muscle (hyperactivity) - bronchodilators (beta2 agonists, muscarnic antagonists)
describe triggers of asthma
allergens
others - exercise, viral infection, smoke, cld, chemicals, drugs (beta - blockers and NSAIDs)
describe the clinical syndrome of asthma
non-smokers early or late onset non-progressive episodic symptoms and signs diurnal variability - nocturnal/early morning non-productive cough, wheeze triggers associated atopy increased IgE (rhinitis, conjunctivitis, eczema) blood eosinophilia>4% responsive to steroids or beta-agonists family history wheezing due to turbulent flow preserved FVC and TLCO normal gas exchange
explain diagnosing asthma
diurnal variation of peak flow rate
reduced forced expiratory ration
reversibility to inh.salbutamol (>15%)
provocation testing - bronchospasm (due to exercise or histamine/metacholine/mannitol)
describe the symptoms of COPD
breathlessness
worsening quality of life
describe the characteristics of disease
decline in exacerbations
reduced lung function
describe COPD - chronic bronchitis and emphysema
chronic bronchitis; chronic neutrophilic inflammation mucus hyper secretion mucocilairy dysfunction altered lung microbiome Smoot muscle spasm and hypertrophy partially reversible
emphysema; alveolar destruction (due to protease imbalance, decrease in protease via smoking or genetically increased production of antiprotease) impaired gas exchange loss of bronchial support irreversible
describe the clinical syndrome of COPD
chronic symptoms (not episodic) smoking non-atopic late onset daily productive cough progressive breathlessness/decline frequent infective exacerbations chronic bronchitis - wheezing emphysema - reduced breath sounds no diurnal variability poor corticosteroid response poor bronchodilator response reduced FVC and TLCO impaired gas exchange neutrolphillic inflammation
