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BRS - Year 2 > **_🫀🫁Cardio & Resp🫀🫁 - Asthma & Respiratory Immunology > Flashcards

**_🫀🫁Cardio & Resp🫀🫁 - Asthma & Respiratory Immunology Flashcards

1
Q

Outline the epidemiology of asthma in the UK

A

5.4 million people in the UK receiving treatment for asthma
1.1 million children
3 people die of an asthma attack every day in the UK
£1billion annual cost to the NHS

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2
Q

What are the cardinal features of presenting asthma?

A

Wheeze +/- dry cough +/- dyspnoea
Episodes of worsening (+/- persistent symptoms) - precipitated by exertion, viral colds, allergen exposure, “high pollution days”
Atopy/allergen sensitisation
Airway inflammation

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3
Q

Which cardinal feature of asthma immediately distinguishes it from COPD?

A

Reversible airflow obstruction - immediate symptomatic relief upon application of a vasodilator

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4
Q

What is the first thing you are looking for if you suspect a diagnosis of asthma?

A

A recurring wheeze

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5
Q

What is the most common form of asthma?

A

Allergic asthma
85-90% of cases

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6
Q

How can you hear a wheeze in asthma?

A

Not always immediately apparent
May only be immediately noticeable in severe cases/during an episode
Baseline may only be detectable with a stethoscope - sometimes not even then

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7
Q

What type of airway inflammation is characteristic of asthma?

A

Type 2 immune reaction - Th2 lymphocytes
Eosinophilia

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8
Q

What is the vague pathogenesis of allergic asthma?

A

Presence of allergen causes airway remodelling (poorly understood, no existing treatments) and inflammation (target of existing treatments)

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9
Q

What produces the wheeze in asthma?

A

Turbulent air flow through constricted airways

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10
Q

What is the difference between a wheeze and stridor?

A

Turbulent airflow from narrowing in lower airways = wheeze
Turbulent airflow from narrowing in upper airways (i.e. an upper airway obstruction above the carina) = stridor

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11
Q

How do asthmatic airways compare to normal airways?

A

Narrower and more inflamed, even at baseline

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12
Q

What is the predominant inflammatory infiltrate in asthma?

A

Eosinophilia

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13
Q

What practical examination can be used to asses airflow obstruction?

A

Spirometry test

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14
Q

What should be looked at in a spirometry test?

A

FEV1/FVC ratio (0.8> in children, 0.7> in adults)
SHAPE of curve

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15
Q

How do people develop asthma?

A

Genetic susceptibility
Polygenic - so is unpredictable, but cannot arise without genetic susceptibility

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16
Q

Why is immunotherapy not a viable treatment for asthma?

A

Too much variety between cases - patients are sensitised to different and often multiple allergens

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17
Q

Outline the immunological cascade that occurs in allergic asthma

A

APCs (dendritic cells in this case) present antigen to Th0 cells
Th0 cells differentiate into Th2 cells (type 2 immunity), with produce lots of IL-4,-5 and -13
Leads to eosinophilia, IgE synthesis and mucus secretion

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18
Q

What are the interleukins produced by Th2 responsible for?

A

IL-13 stimulates mucin secretion
IL-4 stimulates B cells to produce IgE - allergen sensitisation of mast cells and basophils, stimulation of mast cells upon re-exposure
IL-5 - most significant IL - stimulate eosinophilia

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19
Q

What is the result of eosinophilia, in the context of allergic asthma?

A

Release of histamines, cytokines, chemokines, enzymes, growth factors…
Leads to inflammation, bronchoconstriction, airway remodelling etc…

20
Q

How can allergic sensitization be tested?

A

Skin prick tests

21
Q

How can eosinophilia be tested?

A

Blood eosinophil count easiest - >300 cells/mcl is abnormal (in a patient with suspected/confirmed asthma)
Induced sputum eosinophil count: >3% eosinophils is abnormal - can be difficult to obtain
Combine blood eosinophil count with spirometry and skin prick test to come to a diagnosis

22
Q

What exhaled substance can be used as a biomarker of airway (type-2) inflammation?

A

Fraction of exhaled Nitric Oxide (FeNO)
Indirect marker of T2-high eosinophilic airway inflammation in asthma

23
Q

Why is nitric oxide useful for measuring inflammation?

A

Nitric oxide is release by epithelial cells with allergen exposure

24
Q

Briefly outline the asthma diagnosis guideline

A
25
Q

What is the criteria for diagnosis of asthma in children?

A

Symptoms suggestive of asthma
AND
FeNO >35 and positive peak flow variability
OR
Obstructive spirometry and positive bronchodilator reversibility

26
Q

What are the 3 ways of treating asthma?

A

Reduce airway eosinophilic inflammation
Acute symptomatic relief
Severe asthma – steroid sparing therapies

27
Q

What is the main aim of current treatments of asthma?

A

Reduce airway eosinophilic inflammation

28
Q

What is the current treatment for patients with asthma?

A

2 inhalers
Inhaled corticosteroids (extremely effective at reducing eosinophilic inflammation) - baseline treatment taken twice a day
“Blue inhaler” - acute symptomatic relief - Beta-2 agonists (smooth muscle relaxation)
Anticholinergic therapies (smooth muscle relaxation)
Fast acting bronchodilator

29
Q

Currently, what is the biggest problem facing treatment for asthma?

A

Patients not reliably taking their inhaled corticosteroids

30
Q

Why do patients sometimes not take their inhaled corticosteroids?

A

Doesn’t provide immediate symptomatic relief - benefits not immediately felt
Therefore don’t always see the point of taking it every day

31
Q

What issue arises from patients not taking their baseline inhaled corticosteroids?

A

Eosinophilia build up over time, leads to more primed airway to allergen and more severe episodes

32
Q

What are the actions of corticosteroids?

A

Help with nearly every aspect
Main and most potent action is reduced numbers of eosinophils

33
Q

What is the first step for a patient who present with asthma?

A

Immediately prescribe inhaled corticosteroids - regardless of severity

34
Q

What are the most important aspects of asthma managements?

A

Optimal device and technique
Clear asthma management plan - every patient needs their own individual plan
Adherence to inhaled corticosteroids

35
Q

How is the problem of patients not taking their inhaled ICS being solved?

A

Production of a single, combined inhaler
SMART - Single inhaler Maintenance And Reliever Therapy
Same inhaler for maintenance and symptomatic relief during an episode

36
Q

Outline the pathogenesis for an acute asthma attack?

A

Allergens with a combination of pathogens, pollution, tobacco smoke etc…
Triggers immune response
Previous increase of type 2 immunity causes a reduction in type 1 immunity (incl. anti-viral immunity)
Unable to fight cold, marked reduction in lung function, type 2 then gets even more pronounced, eosinophil population skyrockets

37
Q

What is the significance of IgE in allergic asthma?

A

Fundamental allergic immunoglobulin associated with allergic disease/responses

38
Q

Outline anti-IgE antibody therapy

A

Humanised anti-IgE monoclonal antibody
Binds and captures circulating IgE – to prevent interaction with mast cells and basophils to stop allergic cascade
IgE production can decrease with time when patients given anti-IgE Ab
No evidence yet that stopping anti-IgE Ab after some time is a long-term solution

39
Q

What is the main example of anti-IgE antibody therapy?

A

Omalizumab

40
Q

What are the drawbacks of omalizumab?

A

Serum IgE must be between 30-1500 IU/ml - 40% of patients ineligible
Of the remaining 60%, only 50-60% respond to treatment

41
Q

What is mepolizumab?

A

Anti IL-5 antibody - for severe eosinophilic asthma
IL-5 regulates growth, recruitment, activation and survival of eosinophils
Licenced for adults and children >6 years

42
Q

How efficacious is mepolizumab?

A

Clinically significant exacerbations in adults reduced by 50%
Lower efficacy in children - only 25%

43
Q

Which groups of patients respond best to mepolizumab?

A

Patients with elevated blood eosinophils
Higher number of previous exacerbations
Higher dose of inhaled steroids
i.e. more severe asthma

44
Q

What are the current UK recommendations for criteria to use mepolizumab?

A

Severe eosinophilic asthma
Blood eosinophils >300 cells/mcl in the last 12 months
At least 4 exacerbations requiring oral steroids in the last 12 months
Trial for 12 months – 50% reduction in attacks, then continue

45
Q

Why are asthma medications referred to as treatments?

A

NO CURE
Patients will return to baseline immediately upon withdrawal of treatment

BRS - Year 2 (46 decks)

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