Week 4- COPD Flashcards
prevalence of COPD in over 45?
5%
mortality of COPD 10yrs after diagnosis
50%
currently COPD is the – leading cause of disease?
5th, by 2030 its predicted to be the 3rd
Is COPD reversible?
it is both reversible and non reversible, the structural changes cant be undone
Common symptoms of COPD
shortness of breath, wheezing, coughing and increased mucous production
How many die from COPD?
1 in 20
COPD prevalence increases with…
age. 29% of over 75s have COPD
Causes of COPD…
- Smoking
- passive smoking incldued
- life long smokers have a 1 in 2 chance of dev COPD
- number 1 cause of COPD
- Frequent lung infections as a child
- causes decreased lung function
- genetic reasons
- alpha-1 def
- occupational dust and chemicals
- indoor smoke from wood, coals etc.
COPD risk factors
- smoking is a major cause
- cessations slows progression and can be best treatment
- gender
- more males affected than females
- prematurity
- predisposes to childhood chest infections
- asthma
- seems to be an asthma and COPD overlap
- a1 antitrypsin deficiency
- e-cigarettes
Major fetaures of COPD
- Progressive decline in lung functin
- chronic bronchitis
- excessive phelgm/sputum, cough and breahtlessness
- emphysema
- breakdown of alveolar walls, driven by elastase(from neutrophils) induced damage
- *most patients have both
COPD pathology
- emphysema ( disrupted alebolar attachments)
- mucous hypersecretion
- inflammation, fibrosis increase inflammatory cells
- decreased alveoli–> decreased area for exchange –> decreased O2 supply–> feeling of breathlessness
2 COPD presentations
- blue bloater
- clinical diagnosis: daily productive cough for 3 months or more, in at least 2 consecutive years
- overweight and cyanotic(lack of O2)
- elevated haemoglobin because body overcompensating for hypoxia
- peripheral oedema
- rhonchi and wheezing(related to cough)
- pink puffer
- path diagnosis: permanent enlargement and destruction of airspace distal to the terminal bronchiole
- older and thin
- severe dysponea
- quiet chest
- x-ray shows hyperinflation and flattened diaphragm
- makes it harder to breathe out because of increased deadpsaces. the air goes in but doesn’t come out easily
in compariosn to normal lung fucntion, COPD patients…
have a slower rate of expiration, decreased FEV1, reduced peak expiratory flow, and extreme coving. all fo these indicate obstruction
non pharmacological treatments for COPD
assess severity via FEV1, identify and avoid risk factors, cease smoking, flu vaccine, treat co-morbidities, assess exercise capacity
pharmacological treatments for COPD aim to…
- treat symptoms
- prevent exacerbations
- preferably, oral corticosteroids should be limited short-course post-exacerbation
a stepwise approach is recommended, irrespective of disease severity, until adequate control has been achieved
Types of dilators of COPD
- M3 antagonists
- oppose tonic parasymp drive (Ach)
- reduces mucous
- B2-adrenoreceptors agonists
- oppose all contractors
- stimulates mucocillarly clearane
- inhibits release of inflamm mediators from mast cells
- LAMA/LABA
- combination of the 2 is preferred over short acting or single therpaires as we don’t see acute attacks in COPD
- usually for additive dilator effects in COPD
Why are LAMA/SAMAs more important for COPD?
Ach is more important in COPD than other allergic mediators to contract the airways
Averse effects of M3 antagonists
- dry throat( local anti-SLUD)
- acute infection
- flu-like symptoms
- trouble breathing
Adverse effects and limitations of B2 agonists?
- tachycardia via B1
- muscle tremor via B2
- mask inflamm
- potential for receptor down regulation
- densentisation/tolerance
cigarette smoke exposure mouse models
- peristalitic pump cigarette smoke exposure
- nose-only cigarette smoke exposure
- whole body cigarette smoke exposure
After exposing a mouse model to smoke for 3 days…
increased inflammatory cells were found in flushed out lungs, increased cells in lung parenchyma but no remodelling in the short term
cigarette smoke also caused a twitchy contraction and gradual narrowing both to with increased exposure to bronchoconstriction
reduced/impaired relaxation to salbutamol after cigarette smoke exposure. the relaxation is not sustained in exposed models
Corticosteroids for COPD
- Less effective in COPD than in asthma but it is still widely prescribed as we don’t have other treatments
- still targets inflamm but poor efficacy in reducing inflammation due to macrophages and neutrophils
- do not affect symptoms
- inhalation can still reduce frequency and severity of exacerbations
- as eosinophils play a big role in exacerbations
- orally its used to treat exacerbations
- only a short course to minimise adverse side effects
The approved treatment for long term maintenance for moderate to severe COPD is…
daily triple inhaler therapy(LABA/LAMA/ICS)
as severity increases we introduce steroids aswell
a1-antitrypsin deficiency and COPD
Alpha-1-antitrypsin is an endogenous substance that inhibits activity of the trypsin enzyme elastase. If the lungs lack a1-antitrypsin coating it leaves them open for damage by neutrophilic elastase( autodegradation occurs). The mutations means that the a-1-antitrypsin cannot lead the liver and causes liver damage.
a1-antitrypsin replacement therapy
Progression of COPD
Elastase and MMPs in COPD
effects of e-cigarettes
