Flashcards in ASTHMA and COPD Deck (31)
aetiology of airway obstruction in COPD
outside to inside
- alveolar walls
- smooth muscle
what does atopic mean?
characteristics of athma
- airway hyper-responsiveness
- reversible airflow obstruction
- airway inflammation
evolution of asthma
- chronic airway inflammation
- airway remodelling - laying down collagen scar tissue
what happens to the basement membrane during remodelling?
what happens to the submucosa during remodelling?
what happens to the smooth muscle during remodelling?
which interleukin allows TH2 cells to activate B cells?
Which interleukin causes eosinophils to differentiate and activate?
Which interleukins cause mast cells to express IgE receptors?
IL-4 and IL-13
what is the inflammatory cascade in asthma?
1. genetic predisposition
2. eosinophilic inflammation = anti inflammatory medication eg corticosteroids, cromones, theophylline
3. meditaors TH2 cytokines = antileukotrines or antihistamines eg anti-IgE, anti-interleukin-5
4. twitchy smooth muscle (hyperreactivity) = brochodilators eg B2 agonists, muscarinic antagonists
what drugs will melt away eosinophil inflammation and restore mucosal architecture?
clnical syndrome of asthma
- episodic symptoms and signs
- diurinal variability - nocturnal / early morning
- non-productive cough, wheeze
- associated atopy - increased IgE (rhinitis, conjunctivitis, eczema)
- blood eosinophilia > 4%
- repsonsive to steroids or beta agonists
- family history
- wheezing due to turbulent airflow
diagnosis of asthma
- history and examination
- diurinal variation of peak flow rate
- reduced forced expiratory ration (FEV1/FVC < 75%)
- reversibility to inhaled salbutamol (>15%)
- bronchospasm on triggers
COPD disease process
inflammation + mucociliary dysfunction + tissue damage = development of obstruction and ongoing disease progression
characteristics of COPD
- reduced lung function
symptoms of COPD
- progressive breathlessness
- worsening quality of life
- daily productive cough
what happens when you smoke (COPD)?
1. cigarette smoke
2. activated alveolar macrophage release neutrophil chemotactic factor cytokines, mediators,
3. proteases are then released which break down connective tissue and stimulate mucus hyper secretion
4. progressive airflow limitation
these steps lead to emphysema (alveolar wall destruction) and chronic bronchitis (mucus hyper secretion)
- chronic neutrophilic inflammation
- mucus hypersecretiun
- mucociliary dysfunction
- altered lung microbiome
- smooth muslce psam and hypertrophy
- partially reversible
- alveolar destruction
- impaired gas exchange
- loss of bronchial support
asthma COPD overlap syndrome
COPD with blood eosinophils > 4%
- responds better to ICS with regard to exacerbation reduction
- difficult to distinguish between smokers who have airway remodelling
FVC in asthma and COPd
COPD FVC = reduced
asthma FVC = normal
Early or late onset
Non productive cough
Good corticosteroid response
Good bronchodilator response
Preserved FVC and TLCO
Normal gas exchange
No diurnal variability
Poor corticosteroid response*
Poor bronchodilator response
Reduced FVC and TLCO
Impaired gas exchange
what is the diagnosis of sever asthma?
- peak flow <50%
- tachycardia >110bpm
- >25 resp/min
- cant complete sentences
what is the diagnosis of moderate acute asthma?
- increasing symptoms
what is the diagnosis of acute severe asthma?
- PEF 33%-50%
- resp rate > 25
- heart rate > 110
- inability to complete sentences
what is the diagnosis of life-threatening asthma?
- PEF <44%
- O2 < 92%
- altered conscious level
- silent chest
what is panacinar emphysema?
alpha 1 antitrypsin
- resp bronchiole to alveoli enlarged