Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Respiriatory: Airway Disease > Obstructive Airway Disease Overview > Flashcards

Obstructive Airway Disease Overview Flashcards

1
Q

What is an obstructive respiratory disease?

A

Affects the airways

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is a restrictive airway disease?

A

Affects the lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are some examples of obstructive airway diseases?

A
  • Asthma
  • COPD
  • Chronic bronchitis (COPD)
  • Emphysema (COPD)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is asthma?

A

Allergic inflammatory reaction which is usually reversible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is chronic bronchitis (COPD) caused by?

A

Smoking

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is chronic bronchitis characterised by?

A

Neutrophil inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is ACOS?

A

Asthma/COPD overlap syndrome

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Which airways become inflamed in asthma?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are large airways?

A

Diameter larger than 2mm

  • Trachea
  • Bronchi
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are small airways?

A

Diameter less than 2mm

  • Bronchioles
  • Terminal bronchioles
  • Alveolar sacs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Where does the conducting zone end and acinar zone begin?

A

After 17 generation (division)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the conducting zone?

A

Where gas transport takes place

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the acinar/respiratory zone?

A

Where gas exchange takes place

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What airways make up the conducting zone?

A
  • Trachea
  • Bronchi
  • Bronchioles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What airways make up the acinar/respiratory zone?

A
  • Terminal bronchioles

* Alveolar sacs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How many levels of branching does the respiratory tree undergo?

A

23

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

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

A

After 7th generation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is atopic asthma?

A

Individual experiences attacks in response to allergens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is non-atopic asthma?

A

Individual does not experience attacks in response to allergens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is extrinsic asthma?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is intrinsic asthma?

A

No external trigger factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the 3 points the characterise asthma?

A
  • Airway inflammation (characterised by presence of eosinophils)
  • Airway hyper responsiveness
  • Reversible airflow obstruction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What characterises asthmatic inflammation?

A

Eosinophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What characterises inflammation caused by chronic bronchitis (COPD)?

A

Neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is airway hyper responsiveness?

A

Airway becomes sensitive to a variety of abnormal stimuli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What does chronic airway inflammation result in?

A
  • Exacerbation

* Airway hyper-responsiveness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What does airway remodelling result in?

A

Fixed airway obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What does airway remodelling involve?

A

Repair of airways by laying down collagen - permanent obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

How is basement membrane remodelled in asthma?

A

Thickening

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

How is submucosa remodelled in asthma?

A

Collagen deposition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

How is smooth muscle remodelled in asthma?

A

Hypertrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is airway epithelium?

A

Pseudostratified columnar epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Which T cell is involved in asthma?

36
Q

What leukotrienes do TH2 release?

A
  • 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
Q

What are eosinophils used for?

A
  • To fight parasites

* Allergic responses

38
Q

What do eosinophils release in an asthmatic response?

A
  • Basic/catatonic proteins
  • Leukotrienes
  • Cytokines
39
Q

What is the role of IgE released by B cells?

A

Bind to IgE receptors on mast cells, activating them

40
Q

What are useful targets for asthma?

A
  • IgE
  • IL-5
  • Leukotriene D4 (activate more TH2 cells)
  • Histamine (released by mast cells)
41
Q

What is used to treat eosinophilic inflammation?

A

Anti-imflammatory medication

  • Corticosteroids
  • Cromones
  • Theophylline (a methylxanthine)
42
Q

What treatments are used to target mediators or TH2 cytokines?

A
  • Anti-leukotrienes
  • Antihistamines
  • Monoclonal antibodies
  • Anti-IgE
  • Anti interleukin-5
43
Q

What is used to treat hyper-reactivity (twitchy smooth muscle)?

A

Bronchodilators

  • B2 agonists
  • Muscarinic antagonists
44
Q

What is an example of a B2 agonist?

A

Adrenaline/epinephrine

45
Q

Are B2 agonists ever given alone?

A

No, paired with corticosteroids

46
Q

Why are corticosteroids the main asthma treatment?

A

Only treatment proven to reduce inflammation, swelling, and mucus production in the airways

47
Q

What are examples of triggers that symptoms of asthma can occur or worsen in the presence of?

A
  • Allergens
  • Exercise
  • Viral infection
  • Smoke
  • Cold
  • Chemicals
  • Drugs (NSAIDs, B-blockers)

(B-blockers would result in constriction of the airways)

48
Q

What are the signs and symptoms of asthma?

A
  • Episodic symptoms and signs
  • Diurnal variability
  • Non-productive cough
  • Associated atopy (eczema, conjunctivitis, rhinitis)
  • Blood eosinophilia >4%
  • Wheezing due to turbulent airflow
49
Q

Why is it important to take history before testing for asthma?

A

Due to diurnal variability - if test at points in the day where episodes do not occur, will not have wheeze

50
Q

How is asthma diagnosed?

A
  • 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
Q

What are the 3 components of COPD (Chronic Obstructive Pulmonary Disease)?

A
  • Inflammation (characterised by neutrophils)
  • Tissue damage
  • Mucocilliary dysfunction
52
Q

What is COPD caused by?

53
Q

What are the characteristics of COPD?

A
  • Exacerbations

* Reduced lung function

54
Q

What are the symptoms of COPD?

A
  • Breathlessness

* Worsening quality of life

55
Q

How do the airways of someone with COPD differ to normal airways?

A
  • Mucous hyper-secretion (lumen obstruction)
  • Disrupted alveolar attachments (emphysema)
  • Mucosal and peribronchial inflammation and fibrosis (obliterative bronchiolitis)
56
Q

Describe the disease process of COPD

A
  • 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
Q

What cells other than macrophages and neutrophils may also be involved in the COPD inflammatory cascade?

A

CD8+ T cells - involvement in destruction of alveolar wall

58
Q

Why does the COPD inflammatory cascade not occur in normal individuals?

A

Proteases normally counteracted by protease inhibitors

59
Q

What are examples of protease inhibitors?

A
  • a1 - antitrypsin
  • Secretory leukoprotease inhibitor (SLPI)
  • Tissue inhibitors of matrix metalloproteinases
60
Q

Why do protease inhibitors fail to work in COPD?

A

In COPD there appears to be an imbalance between proteases and antiproteases (either an increase in proteases, or a deficiency of antiproteases)

61
Q

What 2 conditions does COPD comprise?

A
  • Chronic bronchitis

* Emphysema

62
Q

What is chronic bronchitis?

A

Chronic neutrophilic inflammation

63
Q

What are the characteristics of chronic bronchitis?

A
  • Mucous hypersecretion
  • Mucocilliary dysfunction
  • Altered lung microbiome
  • Smooth muscle spasm and hypertrophy
  • Partially reversible
64
Q

What does emphysema involve?

A

Alveolar wall destruction

65
Q

What are the characteristics of emphysema?

A
  • Impaired gas exchange
  • Loss of bronchial support
  • Irreversible
66
Q

Are chronic bronchitis and emphysema reversible?

A
  • Chronic bronchitis - partially reversible

* Emphysema - irreversible

67
Q

Why can some individuals smoke for years and never develop COPD?

A

Genetics - higher antiprotenase production

68
Q

How is COPD assessed?

A
  • 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
Q

What are indicators of high risk in COPD?

A
  • 2 exacerbations or more in the past year

* FEV1 <50%

70
Q

What is the ABCD assessment tool for COPD?

A
  • A - less exacerbations, less symptoms
  • B - less exacerbations, more symptoms
  • C - more exacerbations, less symptoms
  • D - more exacerbations, more symptoms
71
Q

What are the symptoms of COPD?

A
  • 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
Q

What can a chronic cascade of COPD result in?

A
  • 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
Q

How can further decline in lung volume in COPD be arrested?

A

Stopping smoking

74
Q

What are characteristics of Asthma COPD Overlap Syndrome (ACOS)?

A
  • COPD with blood eosinophils >4%
  • Responds better to inhaled corticosteroids (ICS)
  • More reversible to salbutamol
75
Q

Why is it difficult to distinguish between COPD and asthmatic smokers?

A

Asthmatic smokers may have airway remodelling i.e. reduced FVC

76
Q

Are asthma and COPD atopic?

A

Asthma - can be atopic

COPD - non-atopic

77
Q

Are asthma and COPD early onset?

A

Asthma - early or late onset

COPD - late onset

78
Q

Are asthma and COPD chronic?

A

Asthma - episodic symptoms

COPD - chronic symptoms

79
Q

Are asthma and COPD progressive?

A

Asthma - non-progressive

COPD - progressive

80
Q

What type of cough is seen in asthma and COPD?

A

Asthma - non-productive

COPD - productive

81
Q

DO asthma and COPD have diurnal variability?

A

Asthma - diurnal variability

COPD - no diurnal variability

82
Q

Do asthma and COPD respond to corticosteroids and bronchodilators?

A

Asthma - good corticosteroid and bronchodilator response

COPD - poor corticosteroid and bronchodilator response

83
Q

How does FVC and TLCO vary in asthma and COPD?

A
  • Asthma - preserved FVC and TLCO

* COPD - reduced FVC and TLCO

84
Q

How is gas exchange affected in asthma and COPD?

A
  • Asthma - normal gas exchange

* COPD - impaired gas exchange

85
Q

What are non-pharmalogical treatments for COPD?

A
  • Stopping smoking
  • Immunisation (exacerbation on infection)
  • Physical activity
  • Oxygen
  • Venesection
  • Lung volume reduction
  • Stenting
86
Q

What are pharmacological treatments of COPD?

A
  • 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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions