Flashcards in Obstructive Airway Disease Deck (112):
what are the 3 conditions which fit into obstructive airway syndrome?
what is COPD/asthma overlap syndromes?
(generally smokers) with features of both asthma and COPD aka COPD with reversibility
what are the 3 parts of 'the asthma triad'?
reversible airflow obstruction
what is the dynamic progression of asthma?
2. chronic airway inflammation
3. airway remodelling
what is involved in the bronchoconstriction stage of asthma?
what is involved in the chronic airway inflammation stage of asthma?
exacerbations and airway hyper-reactivity
what is involved in the airway remodeling stage of asthma?
fixed airway obstruction
what are the 3 hallmarks of airway remodeling?
1. thickening of basement membrane
2. collagen deposition in submucosa
3. hypertrophy of smooth musce
what are the main type of immune cell infiltrate in asthma?
what are the 7 key features of the clinical syndrome of asthma/.
1. episodic symptoms and signs
3. non productive cough, wheeze
5. diurinal variability in episodes
6. associated atopy
7. family history of asthm
what is wheezing in asthma due to?
turbulent airflow in bronchioles
in an asthmatic patient what is the forced expiratory ratio?
FEV1/FVC below 75%
what is a bronchial challenge test?
a method of diagnosis asthma where the patient breathes in either nebulised methacholine (muscarinic agonist) or histamine and the resultant narrowing of airways is detected by spirometry.
how can you tell the difference between a patient without asthma and a patient with asthma on a bronchial challenge test?
patient with asthma will react to much lower doses of the nebulised spasmogens/bronchoconstrictors due to hyperreactivity of the airways
describe the diurnal variability in asthmatic episodes.
increased episodes in the morning morning
(PEFR markedly lower at this times)
how can use use a bronchial challenge test to distinguish between COPD and asthma?
by repeating bronchial challenge test after administration of salbutamol. if there is a reversibility to inhaled salbutamol >15%: asthma
what are the 3 factors involved in the development of obstruction and ongoing disease progression of COPD?
and what are they all caused by?
mucociliary dysfunction inflammation
caused by noxious particles or gases eg smoking
what are the 2 major symtpoms of COPD
what are the 2 major characteristics of the COPD?
reduced lung function
what is the main pathology behind emphysema?
disrupted alveolar attachments
what is the main immune cell involved in the infiltrate within airways in COPD?
what is the main pathology behind chronic bronchitis?
what causes emphysema and chronic bronchitis to occur?
proteases released from stimulated neutrophils causing proteolysis
what are the 4 features of chronic bronchitis?
chronic neutrophilic inflammation
smooth muscle spasm and hypertrophy
what are the 4 features of emphysema?
impaired gas exchange
loss of bronchial support
usually there are protease inhibitors which regulate the proteases produced by stimulated neutrophils, in COPD what happens to these protease inhibitors?
down-regulation causing increase proteolysis
what is the genetic element to acquiring COPD?
deficiency of protease inhibitors
what 3 things must you assess during the assessment of COPD?
assess degree of airflow limitation using spirometry
assess risk of exacerbations
what is an indicator of high risk COPD?
2 + exacerbations in 1 year
FEV1/FVC below 50%
what are the 7 key features of the clinical syndrome of COPD?
1. chronic symptoms (not episodic)
2. daily productive cough
3. increasing breathlessness
5. reduced breath sounds
what causes the wheezing in COPD?
what causes the reduced breath sounds in COPD?
how does a patient with COPD prevent any further decline in lung volume?
what is the inevitable pathway of COPD if patient continues to smke?
1. progressive fixed airflow obstruction
2. impaired alveolar gas exchange
3. respiratory failure (PaO2 decreases, PaCO2 increases)
4. pulmonary hypertension
5. right ventricular hypertrophy/failure (eg cor pulmonale)
why can pulmonary hypertension occur in COPD?
1. emphysema disrupts vascular bed
2. hypoxia causes local vasoconstriction
what are the 7 non-pharmacological ways of managing COPD?
1. smoking cessation
2. immunisation (influenza, pneumococcal)
3. physical activity
4. home oxygen (domiciliary)
(6. lung vol reduction surgery
what are the 7 pharmacological ways of managing COPD?
3. LAMA/LABA combo
4. LABA-ICS combo
(5. PDE4 Inhibitor
6. mucolytic medicine
what mucolytic medicine is occasionally used in COPD?
what PDE4 inhibitor is sometimes used in COPD
compare asthma and COPD in terms of smoking?
compare asthma and COPD in terms of allergy-inducing?
asthma- can be allergic
COPD- always non-allergic
compare asthma and COPD in terms of onset?
asthma- early or late onset
COPD- late onset
compare asthma and COPD in terms of duration of symptoms?
asthma- intermittent symptoms
COPD- chronic symtpoms
compare asthma and COPD in terms of disease progression?
asthma- not progressive
compare asthma and COPD in terms of cough?
asthma- dry cough
COPD- productive cough
compare asthma and COPD in terms of main immune cell mediator?
compare asthma and COPD in terms of daily variability?
asthma- diurnal variability
COPD- no variability
compare asthma and COPD in terms of corticosteroid and bronchodilator response?
asthma- good response in both corticosteroid and bronchodilator response
COPD- poor corticosteroid and bronchodilator response
compare asthma and COPD in terms of FVC and TLCO?
asthma- FVC and TLCO preserved
COPD- reduced FVC and TLCO
compare asthma and COPD in terms of gas exchange?
asthma- normal gas exchange
COPD- impaired gas exchange
what are the 2 main classes of asthma drugs?
what are the 5 stages to the asthma treatment pyramid?
1. SABA PRN
2. Inhaled steroid
3. LABA or theophylline or cysLT receptor antagonist
4. oral steroids
5. anti-IgE monoclonal antibody
what is step 1 of the asthma pyramid for? (SABA prn)
what is step 2 of the asthma pyramid for (inhaled steroid)
mild persistent asthma
what is step 3 of the asthma pyramid for?
(LABA, cystLT RA, theophylline)
moderate persistent asthma
what is step 4 of the asthma pyramid for?
compare therapeutic ratio of prednisolone to beclomethasone?
prednisolone- low therapeutic ratio
beclomethasone- higher therapeutic ratio
how do you optimise lung delivery of an inhaled drug?
use a large volume spacer
what are the 6 benefits of a spacer device?
1. avoids co-ordination problems with MDI
2. reduces oropharyngeal and laryngeal side effects
3. reduced systemic absorption from swallowed fraction
4. acts as a holding chamber for aerosol
5. reduces particle size and velocity
6. improves lung deposition
why is reducing particle size beneficial for inhalation of drugs?
so the drug can get right the way to the alveoli
(remember terminal bronchi are very small)
which type of asthma is cromoglycate especially effective?
why is sodium cromoglycate not used in the treatment of asthma regularly?
what are the 6 main roles of leukotrienes in asthma?
2. increased mucus secretion
3. decreased mucus transport
4. contraction and proliferation of airway smooth muscle
5. eosinophil influx
6. epithelial cell damge
how do leukotrienes cause oedema?
by making blood vessels leaky
how is montelukast administered and how many times daily?
what type of asthma is cysLT receptor antagonists especially effective in?
exercise induced asthma
what is the administration route of H1 receptor antagonists?
what type of asthma are H1 receptor antagonists effective in?
what are H1 receptor antagonists more effective in than asthma?
what is the name of the specific drug used in asthma which is an anti-IgE monoclonal antibody?
how many times is omalizumab injected for treatment of asthma?
one injection every 2-4 weeks
what is step 5 of the asthma pyramid for? (anti-IgE monoclonal antibodies)
severe persistent allergic asthma despite max therapy
what is the disadvantage of using anti IgE monoclonal antibodies for the treatment of asthma?
what is the combination of LABA and ICS used in seretide?
in COPD, how many times daily is the dose of ipratropium? (SAMA)
4 times per day
in COPD, how many times daily is the dose of tiotropium? (LAMA)
1 time per day
in COPD, how many times daily is the dose of aclidinium? (LAMA)
2 times per day
when would ipratropium be used in asthma?
high nebulised doses
how is theophylline administered?
how is aminophylline administered?
what is a xanthine used in the treatment of?
COPD and asthma
how is roflumilast administered?
what is roflumilast a treatment of?
when is roflumilast added to the treatment of a patient with COPD?
as an add on to LABA/LAMA in frequent exacerbations instead of inhaled corticosteroid
what is carbocisteine a treatment of?
COPD (rarely used)
how is carbocisteine administered?
when are antibiotics used within COPD?
for infective exacerbations
what type of infections usually occur in COPR?
endobronchial (infective bronchitis)
rather than alveolar (pneumonia)
what is the empirical 1st line treatment of an infective COPD exacerbation?
doxycycline (covers everything)
amoxicillin (doesnt cover atypicals)
what is the empirical 2nd line treatment of an infective COPD exacerbation?
Clarithromycin, moxifloxacin (will cover stypicals)
in an acute asthma attack what 2 steroid treatment can be given?
if the patient has a falling PaO2 and rising PaCO2 during an asthma attack what does this indicate?
patient is going into respiratroy failure and so needs ITU assisted mechanical intubated ventilation
in addition to steroids what other treatment should be given in an acute asthma attack?
nebulised high dose salbutamol
nebulised high dose ipratropium
+ oxygen 60%
what should you give to a patient who is having an acute COPD attack?
1. nebulised high dose salbutamol + ipratropium
2. oral prednisolone
3. antibiotic (amoxicillin/doxycycline) if infection
4. 24-28% O2 (titrated against PaO2/PaCO2)
5. physio to aide sputum expectoration
6. non invasive ventilation to allow higher FiO2
7. ITU intubated assisted ventilation only if reversible component (eg pneumonia)
what is the epidemiological definition for chronic bronchitis?
cough productive of sputum on most days for 3 months of at least 2 successive years
why is there an increase in mucus production in chronic bronchitis?
defensive mechanism against the chronic irritation
what happens to the small airways in chronic bronchitis?
what happens in respiratory bronchiolitis?
goblet cell metaplasia
fibrosis around bronchioles
what is a marcroscopic image of emphysema?
increase beyond normal in the size of the alveoli (appears as holes in the lung tissue)
what are the 3 general groups of emphysema?
others (eg localised around scars in the lung)
why is there dilation of the alveoli in emphysema?
loss of alveolar walls
where is centriacinar emphysema?
what is centriacinar emphysema caused by?
external factors such as smoking
where is panacinar emphysema?
everywhere in the lungs (including alveoli)
what is panacinar emphysema caused by?
internal factors such as apla 1-anti-trpysin disease
what are the 2 major results of emphysema?
1. diminished alveolar surface area for gas exchange
2. loss of elastic recoil and support of airways leading to tendancy to collapse
what does hypoxia lead to?
increased respiratory rate
what type of protease is elastic tissue in the lung degraded by?
what type of immune cells produce elastase? (and so therefore break down elastic tissue in the lungs- causing emphysema)
neutrophils and macrophages
what does alpha-1 antitrypsin do?
acts as an anti-elastase
(promoting elastin in the lungs)
what does an alpha-1 antitrypsin deficiency cause?
build up of elastase in the lungs (not related to inflammation) and causes the break down of elastin leading to panacinar emphysema