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Respiratory RT > Obstructive Airway Disease > Flashcards

Obstructive Airway Disease Flashcards

1
Q

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

A

asthma
chronic bronchitis
emphysema

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2
Q

what is COPD/asthma overlap syndromes?

A

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

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3
Q

what are the 3 parts of ‘the asthma triad’?

A

reversible airflow obstruction
airway inflammation
airway hyperresponsiveness

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4
Q

what is the dynamic progression of asthma?

A
  1. bronchoconstriction
  2. chronic airway inflammation
  3. airway remodelling
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5
Q

what is involved in the bronchoconstriction stage of asthma?

A

brief symtpoms

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6
Q

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

A

exacerbations and airway hyper-reactivity

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7
Q

what is involved in the airway remodeling stage of asthma?

A

fixed airway obstruction

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8
Q

what are the 3 hallmarks of airway remodeling?

A
  1. thickening of basement membrane
  2. collagen deposition in submucosa
  3. hypertrophy of smooth musce
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9
Q

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

A

eosinophils

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10
Q

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

A
  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
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11
Q

what is wheezing in asthma due to?

A

turbulent airflow in bronchioles

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12
Q

in an asthmatic patient what is the forced expiratory ratio?

A

FEV1/FVC below 75%

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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.

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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

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15
Q

describe the diurnal variability in asthmatic episodes.

A

increased episodes in the morning morning

PEFR markedly lower at this times

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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

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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

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18
Q

what are the 2 major symtpoms of COPD

A

SOB

worsening QoL

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19
Q

what are the 2 major characteristics of the COPD?

A

reduced lung function

exacerbations

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20
Q

what is the main pathology behind emphysema?

A

disrupted alveolar attachments

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21
Q

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

A

neutrophils

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22
Q

what is the main pathology behind chronic bronchitis?

A

mucus hypersecretion

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23
Q

what causes emphysema and chronic bronchitis to occur?

A

proteases released from stimulated neutrophils causing proteolysis

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24
Q

what are the 4 features of chronic bronchitis?

A

chronic neutrophilic inflammation
mucus hypersecretion
smooth muscle spasm and hypertrophy
partially reversible

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25
Q

what are the 4 features of emphysema?

A

alveolar destruction
impaired gas exchange
loss of bronchial support
irreversible

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26
Q

usually there are protease inhibitors which regulate the proteases produced by stimulated neutrophils, in COPD what happens to these protease inhibitors?

A

down-regulation causing increase proteolysis

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27
Q

what is the genetic element to acquiring COPD?

A

deficiency of protease inhibitors

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28
Q

what 3 things must you assess during the assessment of COPD?

A

assess symtpoms
assess degree of airflow limitation using spirometry
assess risk of exacerbations

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29
Q

what is an indicator of high risk COPD?

A

2 + exacerbations in 1 year
or
FEV1/FVC below 50%

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30
Q

what are the 7 key features of the clinical syndrome of COPD?

A
  1. chronic symptoms (not episodic)
  2. daily productive cough
  3. increasing breathlessness
  4. wheezing
  5. reduced breath sounds
  6. smoking
  7. non-atopic
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31
Q

what causes the wheezing in COPD?

A 
chronic bronchitis
(airflow obstruction)
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32
Q

what causes the reduced breath sounds in COPD?

A

emphysema

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33
Q

how does a patient with COPD prevent any further decline in lung volume?

A

stopping smoking

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34
Q

what is the inevitable pathway of COPD if patient continues to smke?

A
  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
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35
Q

why can pulmonary hypertension occur in COPD?

A
  1. emphysema disrupts vascular bed

2. hypoxia causes local vasoconstriction

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36
Q

what are the 7 non-pharmacological ways of managing COPD?

A
  1. smoking cessation
  2. immunisation (influenza, pneumococcal)
  3. physical activity
  4. home oxygen (domiciliary)
  5. venesection
    (6. lung vol reduction surgery
  6. stenting)
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37
Q

what are the 7 pharmacological ways of managing COPD?

A
  1. LAMA
  2. LABA
  3. LAMA/LABA combo
  4. LABA-ICS combo
    (5. PDE4 Inhibitor
  5. mucolytic medicine
  6. antibiotics)
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38
Q

what mucolytic medicine is occasionally used in COPD?

A

carbocisteine

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39
Q

what PDE4 inhibitor is sometimes used in COPD

A

roflumilast

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40
Q

compare asthma and COPD in terms of smoking?

A

Asthma- non-smokers

COPD- smokers

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41
Q

compare asthma and COPD in terms of allergy-inducing?

A

asthma- can be allergic

COPD- always non-allergic

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42
Q

compare asthma and COPD in terms of onset?

A

asthma- early or late onset

COPD- late onset

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43
Q

compare asthma and COPD in terms of duration of symptoms?

A

asthma- intermittent symptoms

COPD- chronic symtpoms

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44
Q

compare asthma and COPD in terms of disease progression?

A

asthma- not progressive

COPD- progressive

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45
Q

compare asthma and COPD in terms of cough?

A

asthma- dry cough

COPD- productive cough

46
Q

compare asthma and COPD in terms of main immune cell mediator?

A

asthma- eosinophils

COPD- neutrophils

47
Q

compare asthma and COPD in terms of daily variability?

A

asthma- diurnal variability

COPD- no variability

48
Q

compare asthma and COPD in terms of corticosteroid and bronchodilator response?

A

asthma- good response in both corticosteroid and bronchodilator response
COPD- poor corticosteroid and bronchodilator response

49
Q

compare asthma and COPD in terms of FVC and TLCO?

A

asthma- FVC and TLCO preserved

COPD- reduced FVC and TLCO

50
Q

compare asthma and COPD in terms of gas exchange?

A

asthma- normal gas exchange

COPD- impaired gas exchange

51
Q

what are the 2 main classes of asthma drugs?

A

preventers (anti-inflammatory)

revlievers (bronchodilators)

52
Q

what are the 5 stages to the asthma treatment pyramid?

A
  1. SABA (salbutamol - blue inhaler)
  2. Add ICS (beclometasone - brown inhaler)
  3. Add LABA (salmeterol - purple inhaler)
    1. Increase ICS dose to max
  5. Add oral SABA OR CysLT1 antagonist (montelukast) OR PDE4 inhibitor (roflumilast, theophylline)
  6. Add Glucocorticoid (oral prednisolone)

If this all fails,anti-IgE antibodies needed (omalizumab)

53
Q

what is step 1 of the asthma pyramid for? (SABA prn)

A

intermittent asthma

54
Q

what is step 2 of the asthma pyramid for (inhaled steroid)

A

mild persistent asthma

55
Q

what is step 3 of the asthma pyramid for?

LABA, cystLT RA, theophylline

A

moderate persistent asthma

56
Q

what is step 4 of the asthma pyramid for?

oral prednisolone

A

severe persistent

57
Q

compare therapeutic ratio of prednisolone to beclomethasone?

A

prednisolone- low therapeutic ratio

beclomethasone- higher therapeutic ratio

58
Q

how do you optimise lung delivery of an inhaled drug?

A

use a large volume spacer

59
Q

what are the 6 benefits of a spacer device?

A
  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
Q

why is reducing particle size beneficial for inhalation of drugs?

A

so the drug can get right the way to the alveoli

remember terminal bronchi are very small

61
Q

which type of asthma is cromoglycate especially effective?

A

atopic asthma

62
Q

why is sodium cromoglycate not used in the treatment of asthma regularly?

A

poor efficacy

63
Q

what are the 6 main roles of leukotrienes in asthma?

A
  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
Q

how do leukotrienes cause oedema?

A

by making blood vessels leaky

65
Q

how is montelukast administered and how many times daily?

A

once daily

oral route

66
Q

what type of asthma is cysLT receptor antagonists especially effective in?

A

exercise induced asthma

67
Q

what is the administration route of H1 receptor antagonists?

A

oral

68
Q

what type of asthma are H1 receptor antagonists effective in?

A

atopic asthma

69
Q

what are H1 receptor antagonists more effective in than asthma?

A

allergic rhinitis

70
Q

what is the name of the specific drug used in asthma which is an anti-IgE monoclonal antibody?

A

omalizumab

71
Q

how many times is omalizumab injected for treatment of asthma?

A

one injection every 2-4 weeks

72
Q

what is step 5 of the asthma pyramid for? (anti-IgE monoclonal antibodies)

A

severe persistent allergic asthma despite max therapy

73
Q

what is the disadvantage of using anti IgE monoclonal antibodies for the treatment of asthma?

A

very expensive

74
Q

what is the combination of LABA and ICS used in seretide?

A

salmeterol/fluticasone

75
Q

in COPD, how many times daily is the dose of ipratropium? (SAMA)

A

4 times per day

76
Q

in COPD, how many times daily is the dose of tiotropium? (LAMA)

A

1 time per day

77
Q

in COPD, how many times daily is the dose of aclidinium? (LAMA)

A

2 times per day

78
Q

when would ipratropium be used in asthma?

A

acute asthma

high nebulised doses

79
Q

how is theophylline administered?

A

oral

80
Q

how is aminophylline administered?

A

IV

acute attacks

81
Q

what is a xanthine used in the treatment of?

A

COPD and asthma

82
Q

how is roflumilast administered?

A

oral

83
Q

what is roflumilast a treatment of?

A

COPD

84
Q

when is roflumilast added to the treatment of a patient with COPD?

A

as an add on to LABA/LAMA in frequent exacerbations instead of inhaled corticosteroid

85
Q

what is carbocisteine a treatment of?

A

COPD (rarely used)

86
Q

how is carbocisteine administered?

A

oral

87
Q

when are antibiotics used within COPD?

A

for infective exacerbations

88
Q

what type of infections usually occur in COPR?

A

endobronchial (infective bronchitis)

rather than alveolar (pneumonia)

89
Q

what is the empirical 1st line treatment of an infective COPD exacerbation?

A 
doxycycline (covers everything)
or 
amoxicillin (doesnt cover atypicals)
90
Q

what is the empirical 2nd line treatment of an infective COPD exacerbation?

A

Clarithromycin, moxifloxacin (will cover stypicals)

91
Q

in an acute asthma attack what 2 steroid treatment can be given?

A

oral prednisolone

IV hydrocortisone

92
Q

if the patient has a falling PaO2 and rising PaCO2 during an asthma attack what does this indicate?

A

patient is going into respiratroy failure and so needs ITU assisted mechanical intubated ventilation

93
Q

in addition to steroids what other treatment should be given in an acute asthma attack?

A 
nebulised high dose salbutamol
\+/-
nebulised high dose ipratropium
\+/- 
aminophylline/Mg
\+ oxygen 60%
94
Q

what should you give to a patient who is having an acute COPD attack?

A
  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
Q

what is the epidemiological definition for chronic bronchitis?

A

cough productive of sputum on most days for 3 months of at least 2 successive years

96
Q

why is there an increase in mucus production in chronic bronchitis?

A

defensive mechanism against the chronic irritation

97
Q

what happens to the small airways in chronic bronchitis?

A

respiratory bronchiolitis

98
Q

what happens in respiratory bronchiolitis?

A

goblet cell metaplasia
macrophage accumulation
fibrosis around bronchioles

99
Q

what is a marcroscopic image of emphysema?

A

increase beyond normal in the size of the alveoli (appears as holes in the lung tissue)

100
Q

what are the 3 general groups of emphysema?

A

centriacinar (centrilobular)
panacinar
others (eg localised around scars in the lung)

101
Q

why is there dilation of the alveoli in emphysema?

A

loss of alveolar walls

102
Q

where is centriacinar emphysema?

A

bronchioles

103
Q

what is centriacinar emphysema caused by?

A

external factors such as smoking

104
Q

where is panacinar emphysema?

A

everywhere in the lungs (including alveoli)

105
Q

what is panacinar emphysema caused by?

A

internal factors such as apla 1-anti-trpysin disease

106
Q

what are the 2 major results of emphysema?

A
  1. diminished alveolar surface area for gas exchange

2. loss of elastic recoil and support of airways leading to tendancy to collapse

107
Q

what does hypoxia lead to?

A

dyspnoea (SOB)
increased respiratory rate
pulmonary vasoconstriction

108
Q

what type of protease is elastic tissue in the lung degraded by?

A

elastases

109
Q

what type of immune cells produce elastase? (and so therefore break down elastic tissue in the lungs- causing emphysema)

A

neutrophils and macrophages

110
Q

what does alpha-1 antitrypsin do?

A

acts as an anti-elastase

promoting elastin in the lungs

111
Q

what does an alpha-1 antitrypsin deficiency cause?

A

build up of elastase in the lungs (not related to inflammation) and causes the break down of elastin leading to panacinar emphysema

112
Q

what 4 things does tobacco smoke cause that predisposes to emphysema?

A
  1. increases number of neutrophils and macrophages in the lungs
  2. slows their transit time
  3. promotes neutrophil degranulation
  4. inhibits alpha 1 antitrypsin

Respiratory RT (10 decks)

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