COPD vs Asthma Flashcards
(26 cards)
Compare the affected site and reactions in them for COPD and Asthma
COPD :
- Small airways and lungs (around 2mm in diameter)
- very little airway hyperresponsiveness
- increased mucus secretion
Asthma
- Large airways
- theres airway hyper responsiveness - triggers that wont normally affect healthy humans
- increased mucus secretion
Contrast the inflammatory cells in COPD and asthma
COPD:
- Neutrophils
- Macrophages
- Tc1 lymphocytes
Asthma
- Eosionphils
- Mast cells
- Th2 lymphocyte
Contrast the mediators for asthma and COPD
COPD:
- TNF-a
- IL-8
- LTB4
Asthma
- IL-4, IL-5
- Cysteine leukotrienes
Compare the treatment for asthma and COPD
Asthma: Brochodilator and corticosteroids will help and reverse the airway obstruction . UNLESS in severe asthma (5%)
COPD
corticosteroids DO NOT WORK
Some Bronchodilator like B2 agonist may be used but it only has a MILD effects
What are the causes of asthma and COPD. Contrast
Asthma - pollutants like pollen etc
COPD
- Smoking
- smoke from cooking (biofuel)
What is the epidemiology of COPD
4th cause of death
5th cause of disability
global increase
What is the epidemiology of asthma
20% children
10% adults
Global increase
Describe how the upper and larger airways are remodelled in asthma
Epithelium thrown into folds due to airway constriction
Mucus plus in airway lumen - this will obstruct the flow of air
What are the 3 diseases that combine to make COPD
Emphysema
Chronic bronchitis - bronchus affected
Chronic bronchiolitis - SMALL AIRWAY DISEASE; affects bronchioles
Describe what happens in chronic bronchitis and SAD
Mucus hypersecretion
fibrosis- hence cant keep airways patent
Describe the gross pathology of an emphysematous Lung
Blackening- due to tar
Ragged edges
Holes in lung slice due to destruction
Describe the overall change in structure of airways and lungs due to chronic bronchitis, SAD and emphysema
Mucus hypersecretion- due to hypertrophy/hyperplasia of submucosal glands and goblet cells
increase in smooth muscle mass BUT NO CONTRACTION
mucosal and peribroncial inflammation and fibrosis (obliterative bronchiolitis)
disrupted alveolar attachments (emphysema)
Do people with COPD have the same severity of its components
NO; they have some of them but in difference abundance and severity
SAD occurs later in COPD stage as its a product of chronic bronchitis
Describe the pathophysiology of COPD
draw it
MCP- monocytes chemoattractant protein
in normal conditions the antioxidants is enough to remove the oxidants. Also the protease inhibitors is enough to balance the effect of proteases
Proteases break down airway walls which would lead to mucus hypersecretion
Describe the effects of smoking on a COPD patient and link it to their lung fucntion (FEV1)
It decreases lung fucntion a lot faster than normal ageing process
Smoking cessation reduce the rate of decline of lung fucntion
Describe the process and results of clinical trials for new drugs for COPD
Require long duration and may have to investigate changes in rate of decline in symptoms
patients would need to have only COPD- no co-morbidities
protease inhibitors are in development for COPD but they’re not a cure although they help to alleviate symptoms
CORTICOSTERIODS AND BRONCHODILATORS DO NOT WORK
Explain the different ways of assessing COPD progression
- Lung function- give baseline of lung capacity
- Bronchoalveolar lavage- fluid put in airways and taken out to see cells/inflammatory signals. This can be uses to see what type and abundance of inflammatory are in airways and lungs.
- High resolution CT scanning- look at lung function- black holes in lungs
Why do small airways become obstructed, stenosed and collapsed
Fibrosis
Hyeprsecretion of mucus- due to more sub mucosal glands and goblet cells
there’s remodelling
Explain what happens to the lung structure during emphysema
Pan acinar - due to reduction in Alpha 1 antitrypsin widespread throughout the lungs
Centriacinar - affects upper lobes. This is due to loss of respiratory bronchioles in proximal part of acinus, hence sparing distal alveoli. This pattern is most typical for smokers.
Why might a protease inhibitor help treat COPD
Reduce activity of protease that lead to remodelling of airways and destruction of lungs. This tries to bring about balance by dampening it’s effects
less mucus made as a result
For people with COPD, why dont endogenous inhibitors work?
There’s not enough and it cant cope with the protease load and hence cant dampen it’s effects
Why use a dual inhibitor (that dampens 2 different proteases)
Double effect- stronger powerful effect in dampening proteases like neutrophil elastase and TIM. Reducing breakdown of lungs
Can allow drug to reach target site at the same time and allow it to be easily regulated
Why might a COPD drug be unlikely to greatly effect disease progression
Differential gene expression and have variation and abundance in proteases. The drug may not have a great inhibitory effect on a particular dominant proteases int he person
What might cause problems with efficacy of inhaled therapy? How can it be solved
There’s already mucus in airways and hence obstruction of drugs and cannot reach target site; mucus is thick.
Can be solved using mucolytics to break down mucus and allow drugs to get to target site
