COPD Flashcards
Why is there a global increase of asthma?
could be because of more diagnosing
or it is actually increasing and we have no reason why
Why is there a global increase in COPD?
increased pollution, climate alteration, smoking/ vaping?
Or is it because of more diagnosing?
What do asthma and COPD have in common?
They are both airway obstructive
roughly 10% have both asthma and COPD
What are the component of asthma?
Reversible
affected site= Large & small airways
Airway hyper-responsiveness
Increased mucus
Inflammatory cells
- Eosinophils
- Mast cells
- Th2 lymphocytes
Mediators
- IL-4, -5, cysLTs
Treatment
- Bronchodilators
- Corticosteroids
What are the component of COPD?
Irreversible
Affected ‘site’= Airways and lung
Very little AHR
Increased mucus
Inflammatory cells
-Neutrophils
- Macrophages
- Tc1 lymphocytes
Mediators
- TNFa, IL-8, LTB4
Treatment, bronchodilators and corticosteroids do not work
What are Tc1 cells?
cytotoxic cells (toxic to cells)
What is asthma pathology?
bronchoconstriction and mucus
epithelium thrown into folds due to airway constriction
mucus plug in airway lumen
What are the 3 types/ aspects of COPD?
chronic bronchitis
Emphysema
Small airway disease
What is chronic bronchitis?
mucus hypersecretion
- main bronchus (extrapulmonary) filled with mucus
- smaller diameter airway
- inflammation
- mucus occluded airways
What is another way of saying small airway disease?
chronic bronchiolitis
Where else can small airway disease occur?
smokers
What is emphysema?
destruction of lung parenchyma and alveoli
What does an emphysematous lung look like?
no clear defined edges
possibly dark due to cigarette
Self digesting (holes from ‘eating itself’)
When might mucolytic therapy work for COPD patients?
mucolytic therapy is thinning of the mucus, so it can be coughed up
- giving temporary relief/ symptom relief (lung function is still bad)
It can work for COPD patients who have more chronic bronchitis than the other aspects of COPD (SAD, emphysema)
What happens during COPD to airways?
Mucosal and peribronchial inflammation and fibrosis (obliterative bronchiolitis)
Mucus hypersecretion (luminal obstruction)
Disrupted alveolar attachments (emphysema)
Increase in size of submucosal gland hypertrophal
Goblet cell hyperplasia (more goblet cells)
How many alveolar macrophages per alveoli?
1 or 2
Do you understand this diagram?
protease inhibors are endogenous (we make them ourselves)
How does lung function change as someone quits smoking, and does it change depending on when you quit?
Why is COPD more common in males and the elderly?
No link between sex and COPD but men started smoking earlier than women so it’s more common in males
Elderly because you usually start smoking when you’re older
What are differences between COPD and asthma?
Asthma and COPD are significant causes of morbidity
COPD is a very significant cause of mortality
Asthma is generally an ‘allergic’ disease
COPD associated with cigarette smoking
Each has a particular ‘portfolio’ of inflammatory cells and inflammatory mediators
Current treatment of asthma (bronchodilators and glucocorticosteroids) generally effective
Current treatment of COPD generally poorly effective
What is the overall pathology, physiology of COPD?
COPD comprises three pathological/pathophysiological features – chronic bronchitis, small airways disease and emphysema
Some features may be more predominant in some patients compared with others
Macrophages, neutrophils, fibroblasts, proteases and oxidants are the ‘major players’ in COPD pathophysiology
Lung function decline in COPD is faster than in non-smokers, and does not return to ‘normal’ upon smoking cessation
What are the basic features of asthma?
Asthma has airway/bronchial hyperresponsiveness – ‘twitchy’ airways to a variety of ‘triggers’ (e.g. cold air) - as a clinical/pathophysiological feature
Mucus hypersecretion in the airways in asthma may exaggerate airway closure due to bronchoconstriction
Bronchodilators dilate the airways – possibly reducing impact of excessive mucus
Describe the linkage between clinical trials and COPD.
Clinical trials in COPD require long duration and may have to investigate changes in rate of decline in symptoms (e.g. lung function)
Trials may include different measurement methodologies
Patients would generally have ‘only’ COPD – no comorbidities
Protease inhibitors are in development for COPD because they have theoretical benefit in treatment, but would not be ‘totally’ effective, nor a ‘cure’
