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Respiratory > Obstructive Diseases > Flashcards

Obstructive Diseases Flashcards

1
Q

Where do obstructive diseases affect?

A

The airways

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2
Q

What are examples of obstructive diseases?

A

Asthma, COPD- chronic bronchitis/emphysema

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3
Q

What is ACOS?

A

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

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4
Q

ACOS is essentially COPD with what?

A

Reversibility and some eosinophilic inflammation which is steroid responsive

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5
Q

Asthma is a chronic inflammatory disease of where?

A

Small and large airways

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6
Q

What is the basic underlying disease process in asthma?

A

Airway inflammation

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7
Q

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

A

23

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8
Q

What is the conducting zone of the bronchial tree?

A

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

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9
Q

What is the respiratory zone of the bronchial tree?

A

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

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10
Q

What zone of the respiratory tree involves the bronchi?

A

Conducting zone

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11
Q

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

A

Respiratory zone

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12
Q

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

A

Small- <2mm, large- >2mm

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13
Q

Where will inhaled particles <5 microns get past?

A

Carina

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14
Q

Where will inhaled particles <2 microns get past?

A

8th branch of bronchioles

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15
Q

What three things must a patient have to have asthma?

A
  • Eosinophilic airway inflammation
  • Airway hyper-responsiveness
  • Reversible airway obstruction
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16
Q

What does bronchoconstriction in asthma cause?

A

Brief symptoms

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17
Q

What does chronic airway inflammation in asthma cause?

A

Exacerbations of asthma

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18
Q

What does airway remodelling in asthma cause?

A

Irreversible fixed airway obstruction

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19
Q

What are triggers treated with in asthma?

A

Allergen avoidance

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20
Q

What is eosinophilic inflammation treated with in asthma?

A

Anti-inflammatory corticosteroids and maybe cromones

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21
Q

What are mediators of asthma and when are they released?

A

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

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22
Q

What medication can be given to block mediators in asthma?

A

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

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23
Q

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

A

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

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24
Q

What are the only drugs which restore normal mucosal architecture?

A

Corticosteroids

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25
Q

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

A

NSAIDs and beta-blockers

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26
Q

How is asthma diagnosed?

A

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

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27
Q

What can COPD lead to?

A

Chronic bronchitis or emphysema

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28
Q

What 5 things can chronic bronchitis cause?

A
  • Mucus hypersecretion
  • Chronic neutrophilic inflammation
  • Mucociliary dysfunction
  • Altered lung microbiome
  • Smooth muscle spasm and hypertrophy
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29
Q

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

A

Emphysema- irreversible

Chronic bronchitis- partially reversible

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30
Q

What are characteristics of COPD?

A

Exacerbations and reduced lung function

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31
Q

What are symptoms of COPD?

A

Breathlessness, cough with sputum production, worsening QOL

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32
Q

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

A

Neutrophil chemotactic factors- IL8 and LTB4

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33
Q

What does neutrophils and macrophages releasing proteases do in COPD?

A

Breaks down connective tissue in the lungs and stimulates mucus hypersecretion

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34
Q

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

A

CD8+ T cells

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35
Q

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

A

Inflammatory changes in the airways including damage of the respiratory mucosa

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36
Q

What is neutrophil elastase?

A

An enzyme which can damage the cilia

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37
Q

What causes the loss of ciliated cells in COPD?

A

Recurrent bacterial infections

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38
Q

How do you assess COPD?

A

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

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39
Q

What are high risk factors for COPD?

A

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

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40
Q

What lung sound will chronic bronchitis show?

A

Wheezing

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41
Q

What lung sound will emphysema show?

A

Reduced breath sounds

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42
Q

What is the chronic cascade in COPD?

A

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

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43
Q

What classifies ACOS?

A

COPD with blood eosinophilia >3%

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44
Q

Will mucosal architecture ever be restored in ACOS?

A

No

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45
Q

Is there reversibility to salbutamol in ACOS?

A

Yes

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46
Q

is there diurnal variability in COPD?

A

No

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47
Q

What do intermittent attacks of bronchoconstriction in asthma result in?

A

Tight chest, wheezing, difficulty breathing, cough

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48
Q

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

A
  • Increase smooth muscle mass
  • Accumulation of fluid (oedema)
  • Increased mucus
  • Epithelial damage
  • Sub-endothelial fibrosis
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49
Q

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

A

Decrease them

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50
Q

What are two bronchial components of asthma?

A

Bronchial hypersensitivity and hyperresponsiveness

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51
Q

What two phases does an asthma attack comprise?

A

Immediate bronchospasm and delayed inflammation

52
Q

Describe the stages of non-atopic asthma?

A

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

53
Q

Describe the stages of atopic asthma?

A

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

54
Q

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

A

Adaptive immune response

55
Q

What do eosinophils differentiate and activate in response to?

A

IL5 from TH2 cells

56
Q

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

A

IL4 and IL13 from TH2 cells

57
Q

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

A

The allergen cross-links the IgE receptor

58
Q

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

A

Intracellular Ca++

59
Q

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

A

Secretory granules containing histamine and more

60
Q

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

A

Release of platelet activating factor and prostaglandins to attract cells

61
Q

What are reliever (bronchodilator) drugs used in asthma?

A

Beta2 agonists, CysLT receptor antagonists

62
Q

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

A

Glucocorticoids, cromones, monoclonal IgE antibodies

63
Q

What asthma drugs have bronchodilator and anti-inflammatory effects?

A

Methylxanthines

64
Q

What is step 1 of asthma treatment?

A

Mild asthma- prescribe SABA to be used as needed

65
Q

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

A

When the SABA is needed more than once daily

66
Q

What is step 2 of asthma treatment?

A

Add inhaled glucocorticoid

67
Q

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

A

Add a LABA

68
Q

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

A

Continue LABA

69
Q

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

A

Increase dose of ICS but keep up LABA

70
Q

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

A

Take off LABA, increase dose of ICS

71
Q

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

A

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

72
Q

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

A

Introduce oral steroid, refer to specialist

73
Q

How do beta adrenoceptor agonists cause smooth muscle relaxation?

A

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

74
Q

What are salbutamol and terbutaline examples of?

A

SABAs

75
Q

When are SABAs taken?

A

As required

76
Q

How are SABAs taken?

A

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

77
Q

How long do SABAs last?

A

They act rapidly and last 3-5 hours

78
Q

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

A

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

79
Q

What are some side effects of SABAs?

A

Fine tremor, tachycardia, dysrhythmia, hypokalaemia

80
Q

What are salmeterol and formoterol examples of?

A

LABAs

81
Q

How long do LABAs last?

A

8 hours roughly

82
Q

What is the most important rule for prescribing LABAs?

A

Never use alone- always co-administer with glucocorticoid

83
Q

Where are CysLT1 receptors usually found?

A

Mast cells and infiltrating inflammatory cells

84
Q

What are montelukast and zafirlukast examples of?

A

CysLT1 receptor antagonists

85
Q

How are CysLT1 receptor antagonists administered?

A

Orally

86
Q

When are CysLT1 receptors not used?

A

For severe, acute relief

87
Q

What are some side effects of CysLT1 receptor antagonists?

A

Headaches, GI disturbance

88
Q

What are theophylline and aminophylline examples of?

A

Methylxanthines

89
Q

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

A

Histone deacetylase

90
Q

What are methyxanthines used in combination with?

A

Beta2 agonist and steroid

91
Q

How are methyxanthines administered?

A

Orally

92
Q

What side effects can methylxathines cause at normal concentrations?

A

Nausea, vomiting, abdominal discomfort and headache

93
Q

What side effects can Methylxanthines cause at high concentrations?

A

dysrhythmias, seizures, hypotension

94
Q

What makes Methylxanthines problematic?

A

Many drug interactions including some antibiotics

95
Q

What is the main glucocorticoid hormone?

A

Hydrocortisone

96
Q

What are glucocorticoids used for in asthma?

A

Prophylaxis

97
Q

How are glucocorticoids usually delivered?

A

Inhaled

98
Q

How do glucocorticoids enter the cell membrane?

A

Diffusion

99
Q

What are some side effects of inhaled glucocorticoids?

A

Hoarse/weak voice, candidiasis

100
Q

When can oral prednisolone be used?

A

In acute, severe, rapidly deteriorating asthma alongside inhaled steroids

101
Q

What are cromones used for?

A

2nd line treatment only really used in children

102
Q

What are cromones often described as?

A

Mast cell stabilisers (suppress histamine release from mast cells)

103
Q

What is an example of a cromone?

A

Sodium cromoglicate

104
Q

What do monoclonal IgE antibodies do?

A

Suppress mast cell response to allergen

105
Q

How are monoclonal antibodies given?

A

IV

106
Q

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

A 
OH- oxygen
S- salbutamol nebulised
H- hydrocortisone IV/oral
I- ipratropium nebulised with salbutamol
T- theophylline
M- magnesium sulphate
AN- anaesthetist
107
Q

What is the acute treatment for COPD? (iSOAP)

A 
I- ipratropium
S- salbutamol
O- oxygen (24-28% in venture mask)
A- antibiotics (amoxicillin if non-severe)
P- prednisolone
108
Q

What 4 things indicate severe asthma?

A

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

109
Q

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

A

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

110
Q

What can treatment for COPD do?

A

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

111
Q

How do muscarinic receptor antagonists work?

A

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

112
Q

What is an example of a SAMA?

A

Ipratropium

113
Q

What is an example of a LAMA?

A

Tiotropium

114
Q

Which receptors does ipratropium block?

A

M1, 2 and 3

115
Q

Which receptor does tiotropium block?

A

M3

116
Q

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

A

M3 and M1 are desirable but M2 is not

117
Q

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

A

Increased FEV1 and smooth muscle relaxation

118
Q

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

A

Pneumonia

119
Q

What are mucolytics such as carbocysteine used for in COPD?

A

To reduce sputum viscosity

120
Q

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

A

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

121
Q

What does O2 therapy do in patients with daytime hypoxaemia?

A

Prolongs life by slowing progression of cor pulmonale

122
Q

How are corticosteroids used in COPD?

A

Combination with a LABA to reduce exacerbations in eosinophilic COPD

123
Q

What can happen if an inhaled drug hits the larynx?

A

Atrophy

124
Q

What is omalizumab?

A

Anti-inflammatory anti-IgE

125
Q

How is omalizumab administered?

A

Injections every 2-4 weeks

Respiratory (16 decks)

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