Lecture outcomes
- Discuss the worldwide prevalence of asthma
- Demonstrate and awareness of the role of genetics in asthma
- Explain the pathophysiology of bronchial asthma
- Describe the remodelling and permanent airways changes in chronic asthma
- Explain causes of exacerbation of asthma
- Have on understanding of occupational asthma
Spectrum of asthma
T2 type asthma allergic asthme and exercise induced asma
late onset eosinoplillic asthma aspirin exacerbated asthma
very late onset asthma (in women)
non t2 type asthma obesity related asthma smoking related asthma smooth muscle mediated paucigrandulocytic asthma
Hereditary of asthma
withone asthmatic parent 3X-6X times as likely 2 then 1x as likely
studies suggest heritable pattern
some genes influence asthma development susceptibility or progression
other genes modify response to therapy
Pathogenesis of asthma
genetics and environmental influences meet to cause early intermittent asthma and all 3 acan lead to chronic asthma
ADAM33 is a gene which is highly involved in chronic airways remodelling
Epigenetic modification in asthma
triggers and causes of asthma
smoking and vaping obesity air pollution allergens viral infections
Th2 cells are highly involved in asthma development
poorly controlled airway inflammtion cold air viral infection tobacco smoke environmental allergens
Asthma pathophysiology
Airway inflammtion
Early phase response type I IgE antibody with mast cells
late phase response Type IV T cell mediated response activates cytokines
Bronchial Hyperresponsiveness
Bronchocontriction
damage to verve endings can lead to bronchospasm
Bronchial wall edema
Excess mucous secretion
Epithelial shedding
Airways remodelling
eosinophil release is toxic to epithelia and can lead to denudation
smooth muscle proliferates
goblet cell hyperplasia matrix deregulation
angiogenesis
histology
eosinophil infilteration mucosal changes etc
cushmans spiral