Obstructive Airway Disease Flashcards
1
Q
what are the 3 conditions which fit into obstructive airway syndrome?
A
asthma
chronic bronchitis
emphysema
2
Q
what is COPD/asthma overlap syndromes?
A
(generally smokers) with features of both asthma and COPD aka COPD with reversibility
3
Q
what are the 3 parts of ‘the asthma triad’?
A
reversible airflow obstruction
airway inflammation
airway hyperresponsiveness
4
Q
what is the dynamic progression of asthma?
A
- bronchoconstriction
- chronic airway inflammation
- airway remodelling
5
Q
what is involved in the bronchoconstriction stage of asthma?
A
brief symtpoms
6
Q
what is involved in the chronic airway inflammation stage of asthma?
A
exacerbations and airway hyper-reactivity
7
Q
what is involved in the airway remodeling stage of asthma?
A
fixed airway obstruction
8
Q
what are the 3 hallmarks of airway remodeling?
A
- thickening of basement membrane
- collagen deposition in submucosa
- hypertrophy of smooth musce
9
Q
what are the main type of immune cell infiltrate in asthma?
A
eosinophils
10
Q
what are the 7 key features of the clinical syndrome of asthma/.
A
- episodic symptoms and signs
- wheezing
- non productive cough, wheeze
- triggers
- diurinal variability in episodes
- associated atopy
- family history of asthm
11
Q
what is wheezing in asthma due to?
A
turbulent airflow in bronchioles
12
Q
in an asthmatic patient what is the forced expiratory ratio?
A
FEV1/FVC below 75%
13
Q
what is a bronchial challenge test?
A
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.
14
Q
how can you tell the difference between a patient without asthma and a patient with asthma on a bronchial challenge test?
A
patient with asthma will react to much lower doses of the nebulised spasmogens/bronchoconstrictors due to hyperreactivity of the airways
15
Q
describe the diurnal variability in asthmatic episodes.
A
increased episodes in the morning morning
PEFR markedly lower at this times
16
Q
how can use use a bronchial challenge test to distinguish between COPD and asthma?
A
by repeating bronchial challenge test after administration of salbutamol. if there is a reversibility to inhaled salbutamol >15%: asthma
17
Q
what are the 3 factors involved in the development of obstruction and ongoing disease progression of COPD?
and what are they all caused by?
A
mucociliary dysfunction inflammation
tissue damage
caused by noxious particles or gases eg smoking
18
Q
what are the 2 major symtpoms of COPD
A
SOB
worsening QoL
19
Q
what are the 2 major characteristics of the COPD?
A
reduced lung function
exacerbations
20
Q
what is the main pathology behind emphysema?
A
disrupted alveolar attachments
21
Q
what is the main immune cell involved in the infiltrate within airways in COPD?
A
neutrophils
22
Q
what is the main pathology behind chronic bronchitis?
A
mucus hypersecretion
23
Q
what causes emphysema and chronic bronchitis to occur?
A
proteases released from stimulated neutrophils causing proteolysis
24
Q
what are the 4 features of chronic bronchitis?
A
chronic neutrophilic inflammation
mucus hypersecretion
smooth muscle spasm and hypertrophy
partially reversible
25
what are the 4 features of emphysema?
alveolar destruction
impaired gas exchange
loss of bronchial support
irreversible
26
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
27
what is the genetic element to acquiring COPD?
deficiency of protease inhibitors
28
what 3 things must you assess during the assessment of COPD?
assess symtpoms
assess degree of airflow limitation using spirometry
assess risk of exacerbations
29
what is an indicator of high risk COPD?
2 + exacerbations in 1 year
or
FEV1/FVC below 50%
30
what are the 7 key features of the clinical syndrome of COPD?
1. chronic symptoms (not episodic)
2. daily productive cough
3. increasing breathlessness
4. wheezing
5. reduced breath sounds
6. smoking
7. non-atopic
31
what causes the wheezing in COPD?
```
chronic bronchitis
(airflow obstruction)
```
32
what causes the reduced breath sounds in COPD?
emphysema
33
how does a patient with COPD prevent any further decline in lung volume?
stopping smoking
34
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)
6. death
35
why can pulmonary hypertension occur in COPD?
1. emphysema disrupts vascular bed
| 2. hypoxia causes local vasoconstriction
36
what are the 7 non-pharmacological ways of managing COPD?
1. smoking cessation
2. immunisation (influenza, pneumococcal)
3. physical activity
4. home oxygen (domiciliary)
5. venesection
(6. lung vol reduction surgery
7. stenting)
37
what are the 7 pharmacological ways of managing COPD?
1. LAMA
2. LABA
3. LAMA/LABA combo
4. LABA-ICS combo
(5. PDE4 Inhibitor
6. mucolytic medicine
7. antibiotics)
38
what mucolytic medicine is occasionally used in COPD?
carbocisteine
39
what PDE4 inhibitor is sometimes used in COPD
roflumilast
40
compare asthma and COPD in terms of smoking?
Asthma- non-smokers
| COPD- smokers
41
compare asthma and COPD in terms of allergy-inducing?
asthma- can be allergic
| COPD- always non-allergic
42
compare asthma and COPD in terms of onset?
asthma- early or late onset
| COPD- late onset
43
compare asthma and COPD in terms of duration of symptoms?
asthma- intermittent symptoms
| COPD- chronic symtpoms
44
compare asthma and COPD in terms of disease progression?
asthma- not progressive
| COPD- progressive
45
compare asthma and COPD in terms of cough?
asthma- dry cough
| COPD- productive cough
46
compare asthma and COPD in terms of main immune cell mediator?
asthma- eosinophils
| COPD- neutrophils
47
compare asthma and COPD in terms of daily variability?
asthma- diurnal variability
| COPD- no variability
48
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
49
compare asthma and COPD in terms of FVC and TLCO?
asthma- FVC and TLCO preserved
| COPD- reduced FVC and TLCO
50
compare asthma and COPD in terms of gas exchange?
asthma- normal gas exchange
| COPD- impaired gas exchange
51
what are the 2 main classes of asthma drugs?
preventers (anti-inflammatory)
| revlievers (bronchodilators)
52
what are the 5 stages to the asthma treatment pyramid?
1. SABA PRN
2. Inhaled steroid
(+/- cromoglycate)
3. LABA or theophylline or cysLT receptor antagonist
4. oral steroids
5. anti-IgE monoclonal antibody
53
what is step 1 of the asthma pyramid for? (SABA prn)
intermittent asthma
54
what is step 2 of the asthma pyramid for (inhaled steroid)
mild persistent asthma
55
what is step 3 of the asthma pyramid for?
| LABA, cystLT RA, theophylline
moderate persistent asthma
56
what is step 4 of the asthma pyramid for?
| oral prednisolone
severe persistent
57
compare therapeutic ratio of prednisolone to beclomethasone?
prednisolone- low therapeutic ratio
| beclomethasone- higher therapeutic ratio
58
how do you optimise lung delivery of an inhaled drug?
use a large volume spacer
59
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
60
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
61
which type of asthma is cromoglycate especially effective?
atopic asthma
62
why is sodium cromoglycate not used in the treatment of asthma regularly?
poor efficacy
63
what are the 6 main roles of leukotrienes in asthma?
1. oedema
2. increased mucus secretion
3. decreased mucus transport
4. contraction and proliferation of airway smooth muscle
5. eosinophil influx
6. epithelial cell damge
64
how do leukotrienes cause oedema?
by making blood vessels leaky
65
how is montelukast administered and how many times daily?
once daily
| oral route
66
what type of asthma is cysLT receptor antagonists especially effective in?
exercise induced asthma
67
what is the administration route of H1 receptor antagonists?
oral
68
what type of asthma are H1 receptor antagonists effective in?
atopic asthma
69
what are H1 receptor antagonists more effective in than asthma?
allergic rhinitis
70
what is the name of the specific drug used in asthma which is an anti-IgE monoclonal antibody?
omalizumab
71
how many times is omalizumab injected for treatment of asthma?
one injection every 2-4 weeks
72
what is step 5 of the asthma pyramid for? (anti-IgE monoclonal antibodies)
severe persistent allergic asthma despite max therapy
73
what is the disadvantage of using anti IgE monoclonal antibodies for the treatment of asthma?
very expensive
74
what is the combination of LABA and ICS used in seretide?
salmeterol/fluticasone
75
in COPD, how many times daily is the dose of ipratropium? (SAMA)
4 times per day
76
in COPD, how many times daily is the dose of tiotropium? (LAMA)
1 time per day
77
in COPD, how many times daily is the dose of aclidinium? (LAMA)
2 times per day
78
when would ipratropium be used in asthma?
acute asthma
| high nebulised doses
79
how is theophylline administered?
oral
80
how is aminophylline administered?
IV
| acute attacks
81
what is a xanthine used in the treatment of?
COPD and asthma
82
how is roflumilast administered?
oral
83
what is roflumilast a treatment of?
COPD
84
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
85
what is carbocisteine a treatment of?
COPD (rarely used)
86
how is carbocisteine administered?
oral
87
when are antibiotics used within COPD?
for infective exacerbations
88
what type of infections usually occur in COPR?
endobronchial (infective bronchitis)
| rather than alveolar (pneumonia)
89
what is the empirical 1st line treatment of an infective COPD exacerbation?
```
doxycycline (covers everything)
or
amoxicillin (doesnt cover atypicals)
```
90
what is the empirical 2nd line treatment of an infective COPD exacerbation?
Clarithromycin, moxifloxacin (will cover stypicals)
91
in an acute asthma attack what 2 steroid treatment can be given?
oral prednisolone
| IV hydrocortisone
92
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
93
in addition to steroids what other treatment should be given in an acute asthma attack?
```
nebulised high dose salbutamol
+/-
nebulised high dose ipratropium
+/-
aminophylline/Mg
+ oxygen 60%
```
94
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)
95
what is the epidemiological definition for chronic bronchitis?
cough productive of sputum on most days for 3 months of at least 2 successive years
96
why is there an increase in mucus production in chronic bronchitis?
defensive mechanism against the chronic irritation
97
what happens to the small airways in chronic bronchitis?
respiratory bronchiolitis
98
what happens in respiratory bronchiolitis?
goblet cell metaplasia
macrophage accumulation
fibrosis around bronchioles
99
what is a marcroscopic image of emphysema?
increase beyond normal in the size of the alveoli (appears as holes in the lung tissue)
100
what are the 3 general groups of emphysema?
centriacinar (centrilobular)
panacinar
others (eg localised around scars in the lung)
101
why is there dilation of the alveoli in emphysema?
loss of alveolar walls
102
where is centriacinar emphysema?
bronchioles
103
what is centriacinar emphysema caused by?
external factors such as smoking
104
where is panacinar emphysema?
everywhere in the lungs (including alveoli)
105
what is panacinar emphysema caused by?
internal factors such as apla 1-anti-trpysin disease
106
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
107
what does hypoxia lead to?
dyspnoea (SOB)
increased respiratory rate
pulmonary vasoconstriction
108
what type of protease is elastic tissue in the lung degraded by?
elastases
109
what type of immune cells produce elastase? (and so therefore break down elastic tissue in the lungs- causing emphysema)
neutrophils and macrophages
110
what does alpha-1 antitrypsin do?
acts as an anti-elastase
| promoting elastin in the lungs
111
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
112
what 4 things does tobacco smoke cause that predisposes to emphysema?
1. increases number of neutrophils and macrophages in the lungs
2. slows their transit time
3. promotes neutrophil degranulation
4. inhibits alpha 1 antitrypsin
