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Respiriatory: Airway Disease > Obstructive Airway Disease Overview > Flashcards

Obstructive Airway Disease Overview Flashcards

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1
Q

What is an obstructive respiratory disease?

A

Affects the airways

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2
Q

What is a restrictive airway disease?

A

Affects the lungs

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3
Q

What are some examples of obstructive airway diseases?

A
  • Asthma
  • COPD
  • Chronic bronchitis (COPD)
  • Emphysema (COPD)
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4
Q

What is asthma?

A

Allergic inflammatory reaction which is usually reversible

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5
Q

What is chronic bronchitis (COPD) caused by?

A

Smoking

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6
Q

What is chronic bronchitis characterised by?

A

Neutrophil inflammation

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7
Q

What is emphysema (COPD)?

A

Emphysema is a condition which causes airflow obstruction but is not a disease of the conducting airways (disease of respiratory airways - alveoli)

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8
Q

What is ACOS?

A

Asthma/COPD overlap syndrome

* Long-standing cigarette smokers who have features of both asthma and COPD

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9
Q

Which airways become inflamed in asthma?

A

Both large airways (trachea, bronchi) and small airways (bronchioles, terminal bronchioles, alveolar ducts/sacs)

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10
Q

What are large airways?

A

Diameter larger than 2mm

  • Trachea
  • Bronchi
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11
Q

What are small airways?

A

Diameter less than 2mm

  • Bronchioles
  • Terminal bronchioles
  • Alveolar sacs
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12
Q

Where does the conducting zone end and acinar zone begin?

A

After 17 generation (division)

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13
Q

What is the conducting zone?

A

Where gas transport takes place

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14
Q

What is the acinar/respiratory zone?

A

Where gas exchange takes place

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15
Q

What airways make up the conducting zone?

A
  • Trachea
  • Bronchi
  • Bronchioles
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16
Q

What airways make up the acinar/respiratory zone?

A
  • Terminal bronchioles

* Alveolar sacs

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17
Q

How many levels of branching does the respiratory tree undergo?

A

23

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18
Q

At what point in the respiratory tree do large airways become small airways?

A

After 7th generation

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19
Q

How does COPD cause airway obstruction?

A
  • Contraction of smooth muscle causes airway to constrict

* Alveolar walls keep respiratory tree open - COPD results in destruction of alveolar walls and bronchial tree collapse

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20
Q

What is atopic asthma?

A

Individual experiences attacks in response to allergens

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21
Q

What is non-atopic asthma?

A

Individual does not experience attacks in response to allergens

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22
Q

What is extrinsic asthma?

A

Has an external trigger factor e.g. allergen, chemical, environmental pollution

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23
Q

What is intrinsic asthma?

A

No external trigger factor

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24
Q

What are the 3 points the characterise asthma?

A
  • Airway inflammation (characterised by presence of eosinophils)
  • Airway hyper responsiveness
  • Reversible airflow obstruction
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25
What characterises asthmatic inflammation?
Eosinophils
26
What characterises inflammation caused by chronic bronchitis (COPD)?
Neutrophils
27
What is airway hyper responsiveness?
Airway becomes sensitive to a variety of abnormal stimuli
28
What does chronic airway inflammation result in?
* Exacerbation | * Airway hyper-responsiveness
29
What does airway remodelling result in?
Fixed airway obstruction
30
What does airway remodelling involve?
Repair of airways by laying down collagen - permanent obstruction
31
How is basement membrane remodelled in asthma?
Thickening
32
How is submucosa remodelled in asthma?
Collagen deposition
33
How is smooth muscle remodelled in asthma?
Hypertrophy
34
What is airway epithelium?
Pseudostratified columnar epithelium
35
Which T cell is involved in asthma?
TH2
36
What leukotrienes do TH2 release?
* IL-4 to activate B cells * IL-13 - used in addition to IL-4 to cause mast cells to express IgE receptors * IL-5 to activate/recruit eosinophils
37
What are eosinophils used for?
* To fight parasites | * Allergic responses
38
What do eosinophils release in an asthmatic response?
* Basic/catatonic proteins * Leukotrienes * Cytokines
39
What is the role of IgE released by B cells?
Bind to IgE receptors on mast cells, activating them
40
What are useful targets for asthma?
* IgE * IL-5 * Leukotriene D4 (activate more TH2 cells) * Histamine (released by mast cells)
41
What is used to treat eosinophilic inflammation?
Anti-imflammatory medication * Corticosteroids * Cromones * Theophylline (a methylxanthine)
42
What treatments are used to target mediators or TH2 cytokines?
* Anti-leukotrienes * Antihistamines * Monoclonal antibodies * Anti-IgE * Anti interleukin-5
43
What is used to treat hyper-reactivity (twitchy smooth muscle)?
Bronchodilators * B2 agonists * Muscarinic antagonists
44
What is an example of a B2 agonist?
Adrenaline/epinephrine
45
Are B2 agonists ever given alone?
No, paired with corticosteroids
46
Why are corticosteroids the main asthma treatment?
Only treatment proven to reduce inflammation, swelling, and mucus production in the airways
47
What are examples of triggers that symptoms of asthma can occur or worsen in the presence of?
* Allergens * Exercise * Viral infection * Smoke * Cold * Chemicals * Drugs (NSAIDs, B-blockers) (B-blockers would result in constriction of the airways)
48
What are the signs and symptoms of asthma?
* Episodic symptoms and signs * Diurnal variability * Non-productive cough * Associated atopy (eczema, conjunctivitis, rhinitis) * Blood eosinophilia >4% * Wheezing due to turbulent airflow
49
Why is it important to take history before testing for asthma?
Due to diurnal variability - if test at points in the day where episodes do not occur, will not have wheeze
50
How is asthma diagnosed?
* History and examination * Diurnal variation of peak flow rate (see-saw pattern) * Reduced forced expiratory ratio (FEV1/FVC <75%) * Reversibility to salbutamol * Provocation testing - bronchospasms (via exercise, histamine/metacholine/mannitol)
51
What are the 3 components of COPD (Chronic Obstructive Pulmonary Disease)?
* Inflammation (characterised by neutrophils) * Tissue damage * Mucocilliary dysfunction
52
What is COPD caused by?
Smoking
53
What are the characteristics of COPD?
* Exacerbations | * Reduced lung function
54
What are the symptoms of COPD?
* Breathlessness | * Worsening quality of life
55
How do the airways of someone with COPD differ to normal airways?
* Mucous hyper-secretion (lumen obstruction) * Disrupted alveolar attachments (emphysema) * Mucosal and peribronchial inflammation and fibrosis (obliterative bronchiolitis)
56
Describe the disease process of COPD
* Cigarette smoke and other irritants activate macrophages and airway epithelial cells in the respiratory tract * Macrophages release neutrophil chemotactic factors - IL-8 and Leukotriene B4 * Neutrophils and macrophages then release proteases * Proteases destroy alveolar wall (emphysema) and result in mucous hyper secretion (chronic bronchitis)
57
What cells other than macrophages and neutrophils may also be involved in the COPD inflammatory cascade?
CD8+ T cells - involvement in destruction of alveolar wall
58
Why does the COPD inflammatory cascade not occur in normal individuals?
Proteases normally counteracted by protease inhibitors
59
What are examples of protease inhibitors?
* a1 - antitrypsin * Secretory leukoprotease inhibitor (SLPI) * Tissue inhibitors of matrix metalloproteinases
60
Why do protease inhibitors fail to work in COPD?
In COPD there appears to be an imbalance between proteases and antiproteases (either an increase in proteases, or a deficiency of antiproteases)
61
What 2 conditions does COPD comprise?
* Chronic bronchitis | * Emphysema
62
What is chronic bronchitis?
Chronic neutrophilic inflammation
63
What are the characteristics of chronic bronchitis?
* Mucous hypersecretion * Mucocilliary dysfunction * Altered lung microbiome * Smooth muscle spasm and hypertrophy * Partially reversible
64
What does emphysema involve?
Alveolar wall destruction
65
What are the characteristics of emphysema?
* Impaired gas exchange * Loss of bronchial support * Irreversible
66
Are chronic bronchitis and emphysema reversible?
* Chronic bronchitis - partially reversible | * Emphysema - irreversible
67
Why can some individuals smoke for years and never develop COPD?
Genetics - higher antiprotenase production
68
How is COPD assessed?
* Assess symptoms * Assess degree of airflow limitation using spirometry * Assess risk of exacerbations * Assess co-morbitdities e.g. Ischaemic heart disease (IHD) and heart failure (HF)
69
What are indicators of high risk in COPD?
* 2 exacerbations or more in the past year | * FEV1 <50%
70
What is the ABCD assessment tool for COPD?
* A - less exacerbations, less symptoms * B - less exacerbations, more symptoms * C - more exacerbations, less symptoms * D - more exacerbations, more symptoms
71
What are the symptoms of COPD?
* Chronic symptoms - not episodic * Non-atopic * Daily productive cough * Progressive breathlessness * Frequent infective exacerbations (worsening of symptoms triggered by viruses etc) * Chronic bronchitis- wheezing * Emphysema - reduced breath sounds
72
What can a chronic cascade of COPD result in?
* Progressive fixed airflow obstruction * Impaired alveolar gas exchange * Respiratory failure: decrease in PaO2, increase in PaCO2 * Pulmonary hypertension * Right ventricular hypertrophy/failure (i.e. Cor Pulmonale) * Death
73
How can further decline in lung volume in COPD be arrested?
Stopping smoking
74
What are characteristics of Asthma COPD Overlap Syndrome (ACOS)?
* COPD with blood eosinophils >4% * Responds better to inhaled corticosteroids (ICS) * More reversible to salbutamol
75
Why is it difficult to distinguish between COPD and asthmatic smokers?
Asthmatic smokers may have airway remodelling i.e. reduced FVC
76
Are asthma and COPD atopic?
Asthma - can be atopic | COPD - non-atopic
77
Are asthma and COPD early onset?
Asthma - early or late onset | COPD - late onset
78
Are asthma and COPD chronic?
Asthma - episodic symptoms | COPD - chronic symptoms
79
Are asthma and COPD progressive?
Asthma - non-progressive | COPD - progressive
80
What type of cough is seen in asthma and COPD?
Asthma - non-productive | COPD - productive
81
DO asthma and COPD have diurnal variability?
Asthma - diurnal variability | COPD - no diurnal variability
82
Do asthma and COPD respond to corticosteroids and bronchodilators?
Asthma - good corticosteroid and bronchodilator response | COPD - poor corticosteroid and bronchodilator response
83
How does FVC and TLCO vary in asthma and COPD?
* Asthma - preserved FVC and TLCO | * COPD - reduced FVC and TLCO
84
How is gas exchange affected in asthma and COPD?
* Asthma - normal gas exchange | * COPD - impaired gas exchange
85
What are non-pharmalogical treatments for COPD?
* Stopping smoking * Immunisation (exacerbation on infection) * Physical activity * Oxygen * Venesection * Lung volume reduction * Stenting
86
What are pharmacological treatments of COPD?
* LAMA or LABA mono * LABA/LAMA combo * ICS/LABA combo * ICS/LABA/LAMA combo (LABA - long acting beta-adrenoceptor agonist) (LAMA - long acting muscarinic antagonists) * PDE4I - Roflumilast * Mucolytic - Carbocisteine * Antibiotics - Azithromycin

Respiriatory: Airway Disease (10 decks)

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