Partial 6 - COPD Flashcards
Which part of airways is affected in asthma, chronic bronchitic and emphysema
Asthma - Large bronchi
Chronic bronchitis - Small bronchi
Emphysema - Alveoli
Risk factors for COPD
1) Exposures; Passive smoking, Ambient air pollution (SO2, NO2), Occupational dust/chemicals, Smoking, socioeconomic status, and childhood infections (PAOSSC)
(2) Host factors; α1-antitrypsin deficiency, hyperresponsive airways, and lung growth.
Effects of smoking (Oxidative stress)
(1) Oxidative stress; Cigarettes contain a lot of oxidants (O2-, OH-, H2O2, HOCl). Fe2+ catalysed production of OH- by neutrophils, eosinophils and alveolar macrophages. Cigarettes contains NO which can react with oxygen and O2- and be converted to nitrates and nitrites including peroxynitrite (O=NOO-) which is a reactive oxygen species.
Effects of smoking (Elastin breakdown)
(2) Elastin breakdown; Activated neutrophils release elastases and oxidants. α1-antitrypsin and metalloproteinase inhibitors (lung defenses) inactivated by smoke. Patients that have deficiency will loose these defences and degradation of elastin decreases elasticity and increases lung compliance
Smoking leads to
- Proinflammatory state with increased expression of pro-inflammatory mediators (IL-8, NF-kB)
- Increased levels of myeloperoxidase and eosinophilic cationic protein leading to bronchoconstriction
- Increased levels of TGF-β which leads to fibrogenesis
- Lipid peroxidation and DNA damage, which lead to epithelial dysplasia and lung cancer.
- Decreased ciliary function, retained secretions, increased airway resistance, and vagal mediated smooth muscle contraction.
- Hypertrophy and hyperplasia of mucus secreting glands and thus increased secretions.
Which pathologies are absent in COPD
Basement membrane thickening
Smooth muscle hypertrophy
Epithelial damage
Which pathologies are absent in Asthma
Alveolar destruction
Physical signs of COPD
(1) Ronchi, which in early disease are present on forced expiration, but later it is present in inspiration and expiration
(2) Prolonged forced expiratory time (>6 sec)
(3) Hyperinflation; With decreased cardiac dullness, liver dullness displaced downward, increased AP chest diameter, decreased heart and breath sounds, Hoover sign (inward movement of the lower rib cage during inspiration
(4) Inspiratory crepitations (lung bases)
(5) Pursed lips breathing (decreases dynamic airway collapse)
(6) Use of accessory respiratory muscles
(7) Signs of cor pulmonale and PHT.
Predominant inflammatory cells in asthma
CD4+ T lymphocytes
Eosinophils
Mast cells
Predominant inflammatory cells in COPD
CD8+ T lymohocytes
Neutrophils
Macrophages
Similarities in COPD and Asthma
(1) Bronchial hyperreactivity
(2) Bronchodilator response
(3) Peripheral blood eosinophilia
(4) Elevated IgE
(5) Eosinophils in the BAL (bronchoscopic alveolar lavage) and airways.
Spirometric classification of COPD
FEV1/FVC ratio < 70%
FEV1 < 80%
Complications of COPD
Hypoxemia, cor pulmonale, hypercapnia and dyspnea
Chronic bronchitis subdivisions
Simple chronic bronchitis
Chronic mucopurulent bronchitis
Chronic bronchitis with obstruction
Chronic bronchitis with obstruction and airway hyperreactivity
Emphysema subdivisions
Centriacinar (centrilobular) where central parts of acini is affected
Panacinar, where the central and peripheral portions of acinus is affected
Paraseptal (distal acinar), where there is distention of alveolar spaces adjacent to septal and pleural surfaces,
Senile emphysema, characterized by enlargement of alveoli and alveolar ducts.