Obstructive Airway Disease Flashcards Preview

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Flashcards in Obstructive Airway Disease Deck (112):
1

what are the 3 conditions which fit into obstructive airway syndrome?

asthma
chronic bronchitis
emphysema

2

what is COPD/asthma overlap syndromes?

(generally smokers) with features of both asthma and COPD aka COPD with reversibility

3

what are the 3 parts of 'the asthma triad'?

reversible airflow obstruction
airway inflammation
airway hyperresponsiveness

4

what is the dynamic progression of asthma?

1. bronchoconstriction
2. chronic airway inflammation
3. airway remodelling

5

what is involved in the bronchoconstriction stage of asthma?

brief symtpoms

6

what is involved in the chronic airway inflammation stage of asthma?

exacerbations and airway hyper-reactivity

7

what is involved in the airway remodeling stage of asthma?

fixed airway obstruction

8

what are the 3 hallmarks of airway remodeling?

1. thickening of basement membrane
2. collagen deposition in submucosa
3. hypertrophy of smooth musce

9

what are the main type of immune cell infiltrate in asthma?

eosinophils

10

what are the 7 key features of the clinical syndrome of asthma/.

1. episodic symptoms and signs
2. wheezing
3. non productive cough, wheeze
4. triggers
5. diurinal variability in episodes
6. associated atopy
7. family history of asthm

11

what is wheezing in asthma due to?

turbulent airflow in bronchioles

12

in an asthmatic patient what is the forced expiratory ratio?

FEV1/FVC below 75%

13

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.

14

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

15

describe the diurnal variability in asthmatic episodes.

increased episodes in the morning morning
(PEFR markedly lower at this times)

16

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

17

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
tissue damage

caused by noxious particles or gases eg smoking

18

what are the 2 major symtpoms of COPD

SOB
worsening QoL

19

what are the 2 major characteristics of the COPD?

reduced lung function
exacerbations

20

what is the main pathology behind emphysema?

disrupted alveolar attachments

21

what is the main immune cell involved in the infiltrate within airways in COPD?

neutrophils

22

what is the main pathology behind chronic bronchitis?

mucus hypersecretion

23

what causes emphysema and chronic bronchitis to occur?

proteases released from stimulated neutrophils causing proteolysis

24

what are the 4 features of chronic bronchitis?

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