Obstructive Diseases Flashcards Preview

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Flashcards in Obstructive Diseases Deck (125):
1

Where do obstructive diseases affect?

The airways

2

What are examples of obstructive diseases?

Asthma, COPD- chronic bronchitis/emphysema

3

What is ACOS?

Asthma/COPD overlap syndrome (smokers with features of both)

4

ACOS is essentially COPD with what?

Reversibility and some eosinophilic inflammation which is steroid responsive

5

Asthma is a chronic inflammatory disease of where?

Small and large airways

6

What is the basic underlying disease process in asthma?

Airway inflammation

7

How many levels of branching does the bronchial tree consist of?

23

8

What is the conducting zone of the bronchial tree?

The first 16-17 branches which play no role in gas exchange

9

What is the respiratory zone of the bronchial tree?

The last 6-7 branches which is where gas exchange takes place

10

What zone of the respiratory tree involves the bronchi?

Conducting zone

11

Which zone of the respiratory tree involves the respiratory bronchioles, alveolar ducts and sacs?

Respiratory zone

12

What is the size roughly of the small and large airways?

Small- <2mm, large- >2mm

13

Where will inhaled particles <5 microns get past?

Carina

14

Where will inhaled particles <2 microns get past?

8th branch of bronchioles

15

What three things must a patient have to have asthma?

- Eosinophilic airway inflammation
- Airway hyper-responsiveness
- Reversible airway obstruction

16

What does bronchoconstriction in asthma cause?

Brief symptoms

17

What does chronic airway inflammation in asthma cause?

Exacerbations of asthma

18

What does airway remodelling in asthma cause?

Irreversible fixed airway obstruction

19

What are triggers treated with in asthma?

Allergen avoidance

20

What is eosinophilic inflammation treated with in asthma?

Anti-inflammatory corticosteroids and maybe cromones

21

What are mediators of asthma and when are they released?

Released upon antigen binding to IgE- histamine, leukotrienes, cytokines

22

What medication can be given to block mediators in asthma?

Anti-histamines/leukotrienes, anti-IgE, anti-IL5

23

What drugs are used to treat hyper-reactive muscle in asthma?

Drugs which stimulate the sympathetic nervous system to relax the airways- bronchodilators, beta2 agonists, muscarinic antagonists

24

What are the only drugs which restore normal mucosal architecture?

Corticosteroids

25

What are the most important drugs to consider as possible causes of asthma?

NSAIDs and beta-blockers

26

How is asthma diagnosed?

History and exam, diurnal variation of peak flow rate, reduced FVC/FEV1 ratio, reversibility to inhaled salbutamol, provocation testing leads to bronchoconstriction

27

What can COPD lead to?

Chronic bronchitis or emphysema

28

What 5 things can chronic bronchitis cause?

- Mucus hypersecretion
- Chronic neutrophilic inflammation
- Mucociliary dysfunction
- Altered lung microbiome
- Smooth muscle spasm and hypertrophy

29

Which out of emphysema and chronic bronchitis is partially reversible and which is irreversible?

Emphysema- irreversible
Chronic bronchitis- partially reversible

30

What are characteristics of COPD?

Exacerbations and reduced lung function

31

What are symptoms of COPD?

Breathlessness, cough with sputum production, worsening QOL

32

What does cigarette smoke cause macrophages and airway epithelial cells to secrete?

Neutrophil chemotactic factors- IL8 and LTB4

33

What does neutrophils and macrophages releasing proteases do in COPD?

Breaks down connective tissue in the lungs and stimulates mucus hypersecretion

34

What might also be involved in the destruction of alveolar wall epithelial cells in COPD?

CD8+ T cells

35

What does an imbalance of proteases and antiproteases lead to in COPD?

Inflammatory changes in the airways including damage of the respiratory mucosa

36

What is neutrophil elastase?

An enzyme which can damage the cilia

37

What causes the loss of ciliated cells in COPD?

Recurrent bacterial infections

38

How do you assess COPD?

Assess symptoms, degree of airflow limitation using spirometry, risk of exacerbations, comorbidities

39

What are high risk factors for COPD?

2 or more exacerbations in one year, <50% FEV1

40

What lung sound will chronic bronchitis show?

Wheezing

41

What lung sound will emphysema show?

Reduced breath sounds

42

What is the chronic cascade in COPD?

Progressive fixed airway obstruction, impaired alveolar gas exchange, type 2 respiratory failure, pulmonary hypertension, cor pulmonale, death

43

What classifies ACOS?

COPD with blood eosinophilia >3%

44

Will mucosal architecture ever be restored in ACOS?

No

45

Is there reversibility to salbutamol in ACOS?

Yes

46

is there diurnal variability in COPD?

No

47

What do intermittent attacks of bronchoconstriction in asthma result in?

Tight chest, wheezing, difficulty breathing, cough

48

Chronic asthma causes changes to the bronchioles as a result of long standing inflammation. What are some examples of these changes?

- Increase smooth muscle mass
- Accumulation of fluid (oedema)
- Increased mucus
- Epithelial damage
- Sub-endothelial fibrosis

49

Airway narrowing and bronchoconstriction in asthma do what to PEFR and FEV1?

Decrease them

50

What are two bronchial components of asthma?

Bronchial hypersensitivity and hyperresponsiveness

51

What two phases does an asthma attack comprise?

Immediate bronchospasm and delayed inflammation

52

Describe the stages of non-atopic asthma?

Allergen, phagocytosis by dendritic cell, low level TH1 response, cell mediated immune response involving IgG and macrophages

53

Describe the stages of atopic asthma?

Allergen, phagocytosis by dendritic cells, strong TH2 response, antibody mediated response involving IgE

54

What does the initial presentation of an antigen stimulate in allergic asthma?

Adaptive immune response

55

What do eosinophils differentiate and activate in response to?

IL5 from TH2 cells

56

What do airway mast cells differentiate and activate in response to?

IL4 and IL13 from TH2 cells

57

What happens on subsequent presentation of an antigen in allergic asthma?

The allergen cross-links the IgE receptor

58

What does cross linking of the IgE receptor in allergic asthma cause release of?

Intracellular Ca++

59

In allergic asthma, what does Ca++ cause release of to cause airway obstruction?

Secretory granules containing histamine and more

60

In allergic asthma, what does Ca++ cause release of to cause inflammation?

Release of platelet activating factor and prostaglandins to attract cells

61

What are reliever (bronchodilator) drugs used in asthma?

Beta2 agonists, CysLT receptor antagonists

62

What are controller/preventer (anti-inflammatory) drugs used in asthma?

Glucocorticoids, cromones, monoclonal IgE antibodies

63

What asthma drugs have bronchodilator and anti-inflammatory effects?

Methylxanthines

64

What is step 1 of asthma treatment?

Mild asthma- prescribe SABA to be used as needed

65

When do patients need to move to step 2 of asthma treatment?

When the SABA is needed more than once daily

66

What is step 2 of asthma treatment?

Add inhaled glucocorticoid

67

If there is still inadequate control, what is step 3 of asthma treatment?

Add a LABA

68

If once added, a LABA is beneficial for asthma, what should you do?

Continue LABA

69

If once added, a LABA is beneficial but not adequate for asthma, what should you do?

Increase dose of ICS but keep up LABA

70

If once added, a LABA is not beneficial for asthma, what should you do?

Take off LABA, increase dose of ICS

71

If asthma is still poorly controlled, what is step 4 of asthma treatment?

Increase dose of ICS and add-on therapy e.g. CysLT1 antagonist, methylxanthine, oral beta2 agonist

72

If still uncontrolled, what is step 5 of asthma treatment?

Introduce oral steroid, refer to specialist

73

How do beta adrenoceptor agonists cause smooth muscle relaxation?

Decrease intracellular Ca++ and activate large K+ conductance channels

74

What are salbutamol and terbutaline examples of?

SABAs

75

When are SABAs taken?

As required

76

How are SABAs taken?

Usually inhaled, can be oral for children and IV for emergencies but these are unlikely

77

How long do SABAs last?

They act rapidly and last 3-5 hours

78

Apart from relaxation of smooth muscle, what other functions do SABAs have?

Increase mucus clearance, decrease mediator release from mast cells and monocytes

79

What are some side effects of SABAs?

Fine tremor, tachycardia, dysrhythmia, hypokalaemia

80

What are salmeterol and formoterol examples of?

LABAs

81

How long do LABAs last?

8 hours roughly

82

What is the most important rule for prescribing LABAs?

Never use alone- always co-administer with glucocorticoid

83

Where are CysLT1 receptors usually found?

Mast cells and infiltrating inflammatory cells

84

What are montelukast and zafirlukast examples of?

CysLT1 receptor antagonists

85

How are CysLT1 receptor antagonists administered?

Orally

86

When are CysLT1 receptors not used?

For severe, acute relief

87

What are some side effects of CysLT1 receptor antagonists?

Headaches, GI disturbance

88

What are theophylline and aminophylline examples of?

Methylxanthines

89

What does theophylline activate to increase anti-inflammatory actions of glucocorticoids?

Histone deacetylase

90

What are methyxanthines used in combination with?

Beta2 agonist and steroid

91

How are methyxanthines administered?

Orally

92

What side effects can methylxathines cause at normal concentrations?

Nausea, vomiting, abdominal discomfort and headache

93

What side effects can Methylxanthines cause at high concentrations?

dysrhythmias, seizures, hypotension

94

What makes Methylxanthines problematic?

Many drug interactions including some antibiotics

95

What is the main glucocorticoid hormone?

Hydrocortisone

96

What are glucocorticoids used for in asthma?

Prophylaxis

97

How are glucocorticoids usually delivered?

Inhaled

98

How do glucocorticoids enter the cell membrane?

Diffusion

99

What are some side effects of inhaled glucocorticoids?

Hoarse/weak voice, candidiasis

100

When can oral prednisolone be used?

In acute, severe, rapidly deteriorating asthma alongside inhaled steroids

101

What are cromones used for?

2nd line treatment only really used in children

102

What are cromones often described as?

Mast cell stabilisers (suppress histamine release from mast cells)

103

What is an example of a cromone?

Sodium cromoglicate

104

What do monoclonal IgE antibodies do?

Suppress mast cell response to allergen

105

How are monoclonal antibodies given?

IV

106

What is the treatment for an acute asthma attack? (OH SHIT MAN)

OH- oxygen
S- salbutamol nebulised
H- hydrocortisone IV/oral
I- ipratropium nebulised with salbutamol
T- theophylline
M- magnesium sulphate
AN- anaesthetist

107

What is the acute treatment for COPD? (iSOAP)

I- ipratropium
S- salbutamol
O- oxygen (24-28% in venture mask)
A- antibiotics (amoxicillin if non-severe)
P- prednisolone

108

What 4 things indicate severe asthma?

Inability to complete sentences, tachycardia, tachypnoea, PEFR < 50% predicted

109

1 or more of what 5 things indicate life-threatening asthma?

PEFR <33% predicted, hypoxaemia, hypercapnia, silent chest, exhaustion

110

What can treatment for COPD do?

Slow, but not reverse disease progression, ease chronic symptoms and prevent acute exacerbations

111

How do muscarinic receptor antagonists work?

By blocking activation of M3 muscarinic receptors by ACh to prevent bronchoconstriction

112

What is an example of a SAMA?

Ipratropium

113

What is an example of a LAMA?

Tiotropium

114

Which receptors does ipratropium block?

M1, 2 and 3

115

Which receptor does tiotropium block?

M3

116

Block of which muscarinic receptors is desirable and which is not?

M3 and M1 are desirable but M2 is not

117

What does a combination of a LAMA and a LABA cause in COPD?

Increased FEV1 and smooth muscle relaxation

118

What risk comes with steroids (particularly oral) in COPD?

Pneumonia

119

What are mucolytics such as carbocysteine used for in COPD?

To reduce sputum viscosity

120

What are PDE4 inhibitors used for in COPD but what are their side effects?

Used to reduce exacerbations but can cause nausea, diarrhoea, headache and weight loss

121

What does O2 therapy do in patients with daytime hypoxaemia?

Prolongs life by slowing progression of cor pulmonale

122

How are corticosteroids used in COPD?

Combination with a LABA to reduce exacerbations in eosinophilic COPD

123

What can happen if an inhaled drug hits the larynx?

Atrophy

124

What is omalizumab?

Anti-inflammatory anti-IgE

125

How is omalizumab administered?

Injections every 2-4 weeks