inflammatory cells activated by allergens -> bronchoconstriction
increased mucous secretion
decreased alveolar ventilation
decreased partial pressure gradients for O2 and CO2
FEV1 = first second of forced expiration
in asthma FEV1 is reduced
FEV1:FVC ratio is reduced
peak expiratory flow is also reduced
B2 agonists cause bronchodilation by increasing intracellular cAMP -> activated PKA and phosphorylation and inactivation of myosin light chain kinases -> inhibits contraction
theophylline = phosphodiesterase inhibitor -> increase in cAMP -> enhance sympathetic activity on airway smooth muscle
anti-muscarinic drugs block vasal effect on airway smooth muscle in asthma
steroids counteract airway inflammation in asthma
leukotriene receptor antagonists block actions of bronchoconstricting and pro-inflammatory leukotrienes
main cause of copd = tobacco smoking
copd = alveolar obstruction (emphysema) and inflammation
airways tend to collapse on expiration
residual volume and TLC is increased causing hypoventilation
chest wall compliance is unchanged in emphysema but lung compliance is increased
causes increased system compliance
FRC higher and closer to chest wall volume
COPD = decreased PEFR, FEV1, FEV1:FVC
classification of COPD is based on FEV1
in COPD there is a large increase in FRC due to increased lung compliance caused by breakdown of the structure of the alveoli and reduced elastic recoil of the lungs
increased RV and decreased VT in COPD, TLC is unchanged
PEF is reduced
managing COPD:
prevent deterioration - no more smoking
bronchodilators to alleviate symptoms and improve exercise capacity
long term O2 therapy to increase partial pressure gradient for O2 by increasing PaO2
fibrosis = increased fibroblast proliferation, increased collagen and elastic -> thickening of alveoli
decreased lung compliance
increased diffusion barrier
dry cough, hypoxaemia and hypocapnia (alveolar ventilation increases to correct hypoxaemia