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BRS YEAR 2 > Cardio - Asthma and Respiratory Immunology > Flashcards

Cardio - Asthma and Respiratory Immunology Flashcards

1
Q

Describe the epidemiology of asthma

A

Affects 5.4 million people in the UK
1 million children affected
3 people die every day in UK
£1 billion spent by NHS annually

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2
Q

What are the 4 cardinal features of asthma

A
  1. Wheeze ± dry cough (+ shortness of breath or dyspnoea)
  2. Allergen sensitisation/atopy
  3. Reversible airway obstruction
  4. Airway inflammation
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3
Q

What may be associated with the dry cough along with the wheeze

A

Worse on exertion, with colds or with allergen exposure

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4
Q

What is associated with airway inflammation

A

Eosinophilia

Type 2 lymphocytes

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5
Q

What are the 3 objective things we use for the diagnosis of asthma

A

Allergen sensitisation/ atopy
Reversible airway obstruction
Airway inflammation

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6
Q

What does a patent airway allow for?

A

Laminar flow of air

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7
Q

What type of airway does an asthmatic have even if they are well without treatment

A

Thickened airway due to wall inflammation and tightened smooth muscles

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8
Q

What causes the wheeze in asthma

A

Turbulent flow

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9
Q

How do we check for reversible airway obstruction

A

Spirometry with the use of bronchodilators

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10
Q

Describe the flow vol loop of an asthmatic

A

We see coving when they patient is breathing out indicating airway obstruction. This is because of an increased resistance in the airway reducing flow rate

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11
Q

What should we see happen in the loop if an asthmatic is given bronchodilators

A

We should see the coving turn into a more straight laminar flow on the FVL

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12
Q

What does the patient need to do when doing spirometry

A

Wear nose clips and do a forced expiratory manoeuvre

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13
Q

What do children need in spirometry

A

Incentive device for cooperation

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14
Q

What do we look for in terms of airway inflammation?

A

Eosinophilia

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15
Q

What is a local allergen challenge?

A

When we inject an allergen directly into the airway of a sensitised asthma patient, we see inflammation, swelling and narrowing of the airway after around 10 minutes

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16
Q

What are the 2 stages of allergic asthma pathogenesis

A
  1. Sensitisation and exposure to allergens

2. Parallel inflammation and remodelling of the airway

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17
Q

With airway remodelling what do we see

A
  • Increased size and number of smooth muscle cells in airway.
  • Increase in matrix size
  • Increase in goblet cells in the epithelium to increase mucus production
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18
Q

In airway inflammation what do we see

A

Recruitment of inflammatory cells, mainly eosinophils

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19
Q

Why do only some people who are sensitised develop asthma?

A

There is genetic susceptibility combined with environmental exposures (allergen, infection, pollution)

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20
Q

What genes may be associated with susceptibility to asthma

A

IL33 and GSDMB - patients have multiple mutations

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21
Q

What type of immunity is associated with allergic asthma?

A

Type 2

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22
Q

How does sensitisation happen in allergic asthma?

A

Inhaled allergen acts as an antigen which is presented to the DCs of the lungs (APC). DCs then carry them to mediastinal lymph nodes where naive Th0 cells differentiate to Th2 to secrete IL4 IL5 IL13.

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23
Q

What does IL5 do

A

Recruits eosinophils and promotes their survival

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24
Q

What does IL4 do

A

Helps the conversion of plasma cells to secrete IgE

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25
Q

What does IL13 do

A

Promotes mucin secretion

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26
Q

After sensitisation, what happens if antigen exposure happens again?

A

Antigen is recognised by specific IgE. These then bind to mast cells to degranulate them and give an allergic reaction

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27
Q

What do mast cells release when degranulated

A

Histamines, eicosanoids, cytokines, chemokines, enzymes, growth factors

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28
Q

What are the 2 main tests for allergic asthma?

A

Skin prick test

IgE test

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29
Q

What is the skin prick test?

A

Intradermal injection of positive control (histamine) and negative control (saline), and then house dust mites, dander etc. We then measure response with wheel and flare

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30
Q

What is the IgE test?

A

We test the blood for specific IgE antibodies

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31
Q

What tests can we use for eosinophilia?

A

Stable blood eosinophil count
Induced sputum eosinophil count
Exhaled nitric oxide

32
Q

What is an abnormal blood eosinophil count when normal

A

≥300 cells/mcl

33
Q

What is an abnormal induced sputum eosinophil count

A

≥2.5% eosinophil

34
Q

What is a contraindication to using exhaled nitric oxide test

A

If they are using steroids

35
Q

What else can FeNO be used for?

A

Measuring compliance of ICS

36
Q

What are the NICE steps for asthma diagnosis?

A

Clinical assessment

Objective tests

37
Q

What do we do in our clinical assessment?

A

History
Examination
Assess/confirm wheeze when they are acutely unwell

38
Q

What are our objective tests?

A

Obstruction - FEv1/FVC
Reversible obstruction- bronchodilator reversibility (BDR)
FeNO

39
Q

What is the diagnosis for FEV1/FVC

40
Q

What is the diagnosis for Bronchodilator reversibility on obstruction?

41
Q

What is the diagnosis for FeNO in adults

42
Q

What is the diagnosis for FeNO in children

43
Q

How many tests do we need to confirm our diagnosis

44
Q

When do we need to test spirometry or peak expiratory flow?

A

We need to test these over 2 weeks to show variability

45
Q

What are the preferred tests for asthma

A

Spirometry

Consider BDR if spirometry shows obstruction

46
Q

If we can’t do BDR or spirometry, what should we do.

A

If child - treat based on prior findings and try again in 6-12 months
If not - consider FeNO

47
Q

If FeNO doesn’t help with diagnosis, what do we do

A

Monitor peak flow variability for 2-4 weeks

48
Q

What is the aim of basic maintenance therapy?

A

Reduce airway inflammation

49
Q

What do we include in basic maintenance therapy?

A
  1. Inhaled corticosteroids (ICS - reduce eosinophils)

2. Leukotriene receptor antagonist - reduces type 2 inflammation

50
Q

What is the aim of acute symptomatic relief?

A

Smooth muscle relaxation

51
Q

What do we include in acute symptomatic relief?

A
  1. Beta-2 agonist

2. Anticholinergic therapies

52
Q

What steroid sparing therapies can we use for severe asthma?

A

Biologics to target IgE or for airway eosinophils

53
Q

What biologics do we have for targeting airway eosinophils

A

Anti IL5 antibody

Anti IL5 receptor antibody

54
Q

What is the prime function of inhaled corticosteroids?

A

Induce apoptosis of eosinophils to reduce inflammation

55
Q

How do ICS affect Th2?

A

Reduce the release of cytokines and mediators

56
Q

How do ICS affect mast cells?

A

Reduce numbers

57
Q

How do ICS affect epithelial cells

A

Reduce cytokines and mediators

58
Q

How do ICS affect endothelial cells

A

Reduce leaking

59
Q

How do ICS affect airway SMC?

A

Reduce cytokines and increase beta receptors

60
Q

How do ICS affect mucus glands

A

Decrease mucus secretion

61
Q

How can we assess adherence accurately?

A

Ensure optimal device and technique, and we can attach an electronic device to their ICC inhaler to measure how often they’re taking the dose

62
Q

What is the threshold for giving ICS ± leukotriene receptor antagonist

A

Even if an adult of child has mild asthma, they are still given maintenance therapy

63
Q

What is a common scenario whereby someone with asthma dies?

A

Someone people fine therefore don’t take their maintenance therapy and suddenly they become exposed to an allergens causing an acute lung attack and thus death in some cases

64
Q

What is the altered immune response underlying an acute lung attack?

A
  1. Increased inflammation, especially alarming (e.g. IL33)
  2. Decreased IFN-1/3 release and response
  3. Increased mast cell degranulation
  4. Increased eosinophil recruitment
  5. Increased mucus production
  6. Decreased CD8 and Th1 responses
  7. Increased Th2 response
  8. Increased viral replication and slower clearance
65
Q

What is the effect of an acute lung attack in school age children

A

Severity of illness is worse:

  • Acute wheeze
  • Eosinophilia is worse
66
Q

How do we treat an acute lung attack

A

High dose of systemic steroids

67
Q

When do we start anti-IgE therapy

A

When there is severe asthma that doesn’t respond to ICS or maintenance therapy

68
Q

What is anti-IgE therapy?

A

Humanised monoclonal anti-IgE antibody that binds to circulating IgE to prevent interaction with mast cells thus preventing the allergic cascade

69
Q

Why may anti-IgE therapy not be used indefinitely?

A

IgE production may decrease over time with biologic therapy therefore there is less need for it

70
Q

What is the criteria for starting someone on Omalizumab?

A
  • Severe persistent IgE mediated asthma
  • 6+ years old
  • Optimised standard therapy w/ no response despite good adherence
  • Frequent exacerbations
71
Q

What are the limitations of omalizumab?

A
  • Need a specific IgE range to start - most people don’t have this (30-1500)
  • Very expensive treatment
72
Q

What is the dosage of omalizumab?

A

Based on weight and serum IgE but normally 2-4 weekly subcutaneous injections

73
Q

What is Mepolizumab?

A

Anti-IL5 antibody that regulates the growth, survival, activation and recruitment of eosinophils.

74
Q

What is mepolizumab used for?

A

It is used for severe eosinophilic asthma

75
Q

What is the criteria for mepolizumab?

A
  • ≥300 eosinophils/mcl in the last year
  • 4 exacerbations in the last 12 months requiring oral steroids
  • After an oral trial for 12 months - you need at least 50% reduction in attacks for continuation
76
Q

How do we know Anti-IL5 antibodies are effective in asthma?

A

DREAm trial showed efficacy of anti IL5 antibodies for severe asthma

BRS YEAR 2 (37 decks)

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