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Block 13 - The Development of Cardiorespiratory Disease > ALS Lecture 5 - The Nature of Airways Obstructions DONE > Flashcards

ALS Lecture 5 - The Nature of Airways Obstructions DONE Flashcards

1
Q

airway obstruction

A

blockage of any part of airway

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2
Q

common obstructive airway diseases (3)

A

asthma, COPD, bronchiectasis

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3
Q

to diagnose airflow obstruction we must use

A

spirometry

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4
Q

label the spirometry diagram (A)

A

done

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5
Q

FEV1

A

forced expiratory capacity in 1 second (amount of air blown out in 1sec)

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6
Q

FVC

A

forced vital capacity, total amount of air you can blow out

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7
Q

FEV1:FVC ratio should be

A

> 70%

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8
Q

FEV1:FVC ratio <70% =

A

diagnosed obstruction

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9
Q

if FEV1 and FVC are symmetrically decreased (ratio is still normal) then =

A

diagnosed restriction

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10
Q

label the diagrams of mechanisms of airflow obstructions (B)

A

done

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11
Q

3 mechanisms of airflow obstruction

A

mucus, constricted smooth muscle, supporting structure damage

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12
Q

increased secretions/mucus in airways obstruction

A

cough may clear

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13
Q

constricted smooth muscle obstruction

A

asthma, bronchitis

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14
Q

supporting structure damage obstruction

A

alveoli collapse in emphysema

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15
Q

bronchial hyper reactivity is a measure of airway

A

‘twitchiness’

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16
Q

the ‘twitchier’ the airways, the

A

harder to control

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17
Q

asthmatic airways are very

A

sensitive

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18
Q

label the flowchart (C)

A

done

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19
Q

bronchial hyperactivity can be assessed with a

A

bronchial challenge test

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20
Q

most often used products in bronchial challenge test (2)

A

methacholine, histamine

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21
Q

chemicals used in bronchial challenge test trigger a bronchospasm in normal individuals but people with _____ ___ ______ have a ____ ____

A

bronchial hyper responsiveness, lower threshold

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22
Q

bronchial hyper responsiveness is usually found in (2)

A

asthma, COPD

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23
Q

PC20 =

A

point where FEV1 drops by 20%

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24
Q

lower PC20 =

A

worse asthma

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25
Q

look at the diagrams of bronchial challenge testing (D)

A

done

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26
Q

asthma is usually characterised by (3)

A

reversible airflow obstruction, chronic airway inflammation, increased airway responsiveness

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27
Q

chronic airway inflammation is mostly

A

eosinophilic

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28
Q

asthma is commonly divided into 2 types

A

atopic (extrinsic), non-allergic (intrinsic

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29
Q

atopic/extrinsic asthma is characterised by symptoms that are triggered by an

A

allergic reaction

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30
Q

non-allergic/intrinsic asthma is triggered by factors not related to

A

allergens

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31
Q

how many children get asthma?

A

1/6

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32
Q

how many children grow out of asthma?

A

50%

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33
Q

variable airflow obstruction

A

> 50% increase of FEV1 following bronchodilator use

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34
Q

2 types of T lymphocytes in asthma

A

T helper 1, T helper 2

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35
Q

T helper 1 promote cell immunity by (2)

A

IgG production, gamma interferon

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36
Q

T helper 2 promote immunity by (3)

A

enhancing mast cells and eosinophils, IgE synthesis

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37
Q

in asthma there is more __ activity than __

A

more Th2 than Th1

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38
Q

label the diagram of asthma (E)

A

done

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39
Q

mechanism of atopic asthma (7 steps)

A
  1. APC present antigen to T cell
  2. Th2 cells produce IL-4, IL-5, IL-13
  3. interleukins signal B cells to produce IgE
  4. IgE recognises allergen, binds to mast cells in airway
  5. with antigen, IgE causes mast cell degranulation
  6. degranulation of mast cells release inflammatory mediators like histamine, leukotrienes that promote bronchospasm
  7. cytokines attract eosinophils (more inflammation)
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40
Q

IL-4 in asthma

A

stimulates IgE production

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41
Q

IL-5 in asthma

A

activates recruited eosinophils

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42
Q

IL-13 in asthma

A

activates mucus secretion, promotes IgE

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43
Q

4 main asthma phenotypes

A

atopic, non-allergic, obesity, persistent airflow limitation

44
Q

atopic asthma (3)

A

childhood, eosinophils, identifiable triggers

45
Q

non-allergic asthma (2)

A

eosinophilic, neutrophilic?

46
Q

persistent airflow limitation asthma (2)

A

fixed obstruction or incompletely reverses

47
Q

asthma and obesity (2)

A

prominent respiratory symptoms, little evidence of eosinophils

48
Q

asthma triggers (6)

A

pets, dust, mould, pollen, occupational, food

49
Q

atopy pathophysiology (4 steps)

A
  1. first allergen exposure, IgE antibodies bind to mast cells and basophils
  2. same allergen reenters, attaches to IgE
  3. mast cells and basophils release histamines
  4. more smooth muscle contraction and mucus
50
Q

objective evidence of atopy (3)

A

total IgE blood, specific IgE to aeroallergens (RAST) blood, skin prick

51
Q

acute asthma airway changes (5)

A

smooth muscle contraction, mucus, plasma leak, oedema, sensory nerve activation

52
Q

chronic asthma airway changes (2)

A

subepithelial fibrosis, smooth muscle hypertrophy

53
Q

diagnosis of asthma (3)

A

variable airway narrowing, bronchodilator reversibility study, peak flow

54
Q

look at the diagram of asthma flow chart (F)

A

done

55
Q

PEFR monitoring (2)

A

depends on meter, effort

56
Q

reversibility testing (2)

A

pre- and post- bronchodilator spirometry

57
Q

when is reversibility testing considered positive?

A

FEV1 increases by 200mls

58
Q

gold standard in asthma diagnosis testing

A

sputum eosinophilia

59
Q

treatment for asthma that works in most people (2)

A

corticosteroids, bronchodilators

60
Q

if an asthmatic is highly atopic (too much IgE we can use drugs such as (1)

A

Omalizumab

61
Q

in asthma we can also use IL-5 blockers such as (1)

A

Mepoluzimab

62
Q

label the flow chart of asthma medications (G)

A

done

63
Q

reasons patient may not be getting better with asthma treatment (3)

A

poor compliance, poor technique, misdiagnosis

64
Q

COPD is characterised by (3)

A

slow progression, air trapping, airflow limitation

65
Q

main risk factor for COPD

A

smoking

66
Q

label the FEV1 COPD diagram (H)

A

done

67
Q

types of COPD (2)

A

chronic bronchitis, emphysema

68
Q

obstructive bronchitis

A

small airway disease

69
Q

emphysema

A

breakdown of lung tissue

70
Q

chronic bronchitis involves (5)

A

mucus gland hypertrophy, smooth muscle hypertrophy, goblet cell hyperplasia, inflammatory cell infiltrate, excess mucus

71
Q

in chronic bronchitis inflammatory cell infiltrates are

A

lymphocytes, neutrophils

72
Q

emphysema involves (3)

A

enlargement of airspace distal to terminal bronchiole, fibrosis, wall destruction

73
Q

2 major types of emphysema

A

centrilobular, panlobular

74
Q

centrilobular emphysema (3)

A

upper lobes, proximal acinus of bronchiole, spared distal alveoli

75
Q

panlobular emphysema (2)

A

all lung fields, loss of all portions from bronchiole to alveoli

76
Q

label the diagram of emphysema types (I)

A

done

77
Q

on emphysema scans, lung destruction is more marked in

A

upper zones

78
Q

emphysema CT scans show (2)

A

emphysematous bulla, squashes normal lung

79
Q

look at scans of emphysema (J)

A

done

80
Q

lebel the diagram of the normal airway and airway in emphysema (K)

A

done

81
Q

how does emphysema cause airflow obstruction (2 steps)

A
  1. alveolar pressure = pleural pressure + elastic recoil

2. reduced pressure and traction in emphysema

82
Q

label the flow chart of vicious cycle of inactivity and symptoms (L)

A

done

83
Q

COPD and inactivity (3 steps)

A
  1. airflow obstruction worsened by exacerbations
  2. air trapping
  3. hyperinflation, breathlessness
  4. limited activity = less fitness = less muscle
  5. increased breathing rate
84
Q

causes of COPD (6)

A

smoking, drugs, chronic asthma, occupations, familial, passive smoking

85
Q

diagnosis of COPD

A

FEV1:FVC doesn’t improve by 20% with bronchodilator

86
Q

2 phenotypes in COPD patients

A

blue bloaters, pink puffers

87
Q

blue bloater has predominantly

A

bronchitis

88
Q

blue bloaters symptoms (5)

A

sputum, oedematous ankles, cyanosed, overweight, sleep apnoea

89
Q

blue bloaters go into ______ ____ early on in natural history of disease

A

ventilatory failure

90
Q

pink puffer has predominantly

A

emphysema

91
Q

pink puffer symptoms (3)

A

thin, pursed lip breathing, accessory muscle use

92
Q

look at the Fletcher-Peto plot and label it (M)

A

done

93
Q

fill in the table of asthma and COPD (N)

A

done

94
Q

label the venn diagram of COPD and asthma (O)

A

done

95
Q

label the diagram of flow through the airway (P)

A

done

96
Q

resistance =

A

inversely proportional to radius4

97
Q

airflow obstruction can cause hypoxia due to (2)

A

ventilation perfusion mismatch, poorly ventilated alveoli due to bronchial narrowing

98
Q

pulmonary hypertension is a bad sign in

A

COPD

99
Q

pulmonary hypertension is improved by

A

long term O2 therapy

100
Q

consequence of pulmonary hypertension

A

cor pulmonale

101
Q

cor pulmonale

A

right sided heart failure, usually due to chronic lung disease

102
Q

bronchiectasis is a disease in which there is a permanent

A

enlargement of parts of airways

103
Q

most common cause of bronchiectasis

A

cystic fibrosis

104
Q

symptoms of bronchiectasis (3)

A

bronchial dilation, recurrent infection, chronic purulent sputum

105
Q

other causes of bronchiectasis (5)

A

immunodeficiency, rheumatoid arthritis, colitis, post-measles, idiopathic

106
Q

bronchiectasis CT scan of lungs

A

signet ring sign, dilated bronchiole

Block 13 - The Development of Cardiorespiratory Disease (14 decks)

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