asthma Flashcards

1
Q

what is the Britsh thoracic society’s definition of asthma

A

Clinical diagnosis
No consistent gold standard diagnostic criteria
Central to diagnosis is presence of symptoms (more than one of wheeze, breathlessness, chest tightness, cough and variable airflow obstruction)
Heterogenous disease characterised by chronic airways inflammation

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2
Q

how does WHO define asthma

A

Is a disease characterised by recurrent attacks of breathlessness, wheezing which vary in sev and freq from person to person. May occur hour to hour or day to day.

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3
Q

how is asthma diagnosed

A

Combo of clinical assessment, objective tests but symptoms can change

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4
Q

why is asthma important

A

315 million adults worldwide

340,000 deaths a year

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5
Q

what is the impact of asthma

A

5.4 million people are currently being treated for the condition in the UK
On avg 3 people die a day from an asthma attack in UK (185 admissions a day)
NHS spends about a billion on treatment and care
In 2017 1484 died in UK, 50% increase compared to EU

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6
Q

what is the natural history of asthma

A

Most commonly presents in childhood or middle age
50% of kids with mild asthma may grow out of it by 21 (minority returns years later)
70% of kids with persistent asthma with have symptoms in adult life
Adult onset more likely to persist

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7
Q

what are causes of airflow obstruction

A

Bronchoconstriction – contraction of the smooth muscle in the bronchial wall
Bronchial secretions and plugs of mucus – due to inflammation of the bronchial wall
Oedema of the bronchial wall due to inflammation in the lining mucosa of bronchial wall

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8
Q

how do normal airways compare to asthmatic airways

A

narrower due to widened epithelium and smooth muscle (constriction)
mucous plug
enlarged mucous glands

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9
Q

what is atopy

A

Asthma in young people usually inked to atopy
Tendency to form IgE antibodies to allergens
Often associated hay fever or eczema in personal or family history

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10
Q

what is the pathophysiology of asthma

A

antigens activate immune system, causing an inflammatory cascade, bronchoconstriction and inflammation (chemokine recruiting mast cells and eosinophils)

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11
Q

what are the symptoms of asthma

A

Cough
Wheeze
Breathlessness
Chest tightness
Occurs in episodes with periods of no (or minimal symptoms)
Diurnal variability so worse at night or early morning

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12
Q

what medications can trigger asthma

A

aspirin
ibuprofen
beta blockers

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13
Q

what are triggering factors of asthma

A

inflammation - resp infections, allergens, work place
constriction - change in temp, exercise, cold air, emotion and stress, strong odours
others- medications, tobacco, reflux, air pollution, food additives

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14
Q

how can asthma be diagnosed

A

History is crucial – mor than one symptom
Symptom free periods
Past medical history
Family history
Social history
Alternative diagnosis – unlikely but what else could present similarly
Physical exam (except during an attack)

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15
Q

what asthma investigations are done by a gp

A

Peak flow monitoring twice a day for two weeks

Spirometry may show airflow obstruction – could be normal between attacks

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16
Q

what asthma investigations are done by a gp/hospital

A

Chest Xray often normal but may = hyperinflation
Inc eosinophil count in blood
Fraction exhaled nitric oxide (FeNO)
Tests done by hospital
Skin prick or blood tests may confirm allergies

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17
Q

what are tests of lung function

A

Is there airflow obstruction (FEV1/FVC ration <70)
Vary over time
PEFR monitoring – 20% diurnal variation
Reversible
With bronchodilators (salbutalmol, 15% and 200 mls improvement in FEV1 from baseline)

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18
Q

how is PEFR monitoring done

A

best of 3

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19
Q

what is FeNO

A

fraction of exhaled nitric oxide
Measure of airways eosinophilic inflammation
Performed on patients not on any treatment, a positive test (>40ppb) supports diagnosis
Can be done in GP or hospital clinics
Can be used to monitor treatment/look at compliance

20
Q

How can asthma be managed long term, non pharmacologically

A

Smoking cessation
Weight reduction
Pollution (provoke or exacerbate but effects of allergens, smoking and infection more sig)

21
Q

How can asthma be managed long term, pharmacologically

A

Control of disease (preventers)
Inhaled corticosteroids (ICS)
Key part of first line treatment (eg beclometasone, fluticasone, budesonide, ciclesonide)

22
Q

what are Inhaled long acting beta 2 agonists (LABA)

A

Formoterol, salmeterol
In combo with ICS as add on if still symptomatic
Never a single agent treatment alone, ass with inc deaths

23
Q

how can asthma be treated orally (long term)

A

Oral leukotriene antagonist montelukast
Oral theophyllines
In patients with chronically poorly controlled asthma, low dose long term oral steroids by hospital direction

24
Q

what are Short acting beta agonists (SABA)

A

Short/immediate relief of symptoms (relievers)

Salbutamol, terbutaline as inhaler (Sal 100mcg) or nebuliser (high dose salbutamol 2.5mg driven by oxygen)

25
Q

what is maintenance and reliever therapy (MART)

A

LABA formoterol short onset of action, equiv to salbutamol
So certain ICS/LABA combos can be relievers too
Pts take additional doses ( 4 a day) for short periods (2-3 days) to rapidly treat any worsening asthma symptoms
Aiming to address inflammatory aspect by having both ICS and LABA

26
Q

What are the BTS guidelines for asthma

A

reg preventer - low dose ICS
initial add-on therapy - add inhaled LABA to ICS (fixed dose or MART)
Additional controller therapies
inc ICS to med dose or adding LTRA (+ if no response to LABA then stop it)
Specialist therapies

27
Q

what are the two different inhaler devices

A

DPIs and pMDIs

28
Q

what are DPIs

A

dry powder inhalers
activated by inspiration by patient
powdered drug dispersed into particles by inspiration
53-59% effective when used correctly

29
Q

what are pMDIs

A

pressurised metered dose inhalers
drug dissolved into propellant HFCs under pressure, valve system releases metered dose
23-43% effective without spacer, with 55-57%

30
Q

how is inhaler to use decided

A

Where they are in treatment eg stepping up from ICS to ICS/LABA
What device they can use eg dexterity and inspiratory flow
Side effects eg oral candidas/thrush (ICS), tremor and tachycardia (SABA/LABA)
What device they want to use eg carbon footprint
Counter so they know how many doses left
Cost

31
Q

what are specialist treatment

A

for a small number of patients with difficult asthma Monoclonal antibodies (anti IgE injections omalizumab or anti IL5 treatment mepolizumab)

32
Q

what are unintentional barriers to treatment adherence

A
Misunderstanding 
Poor inhaler technique 
Language
Forgetfulness
Stress
33
Q

what are intentional barriers to treatment adherence

A

Concern about side effects
Denial
Cost

34
Q

how can asthma basely managed

A

List daily medications and explain
List triggers to avoid, importance of smoke free environment
Look for deterioration signs, PEFR
Names and doses to treat worsening asthma
Indicators of how and when to seek medical attention
Easy to understand, 2-3 action points, traffic light colour coded

35
Q

what does a PAAP do (personal asthma action plan)

A

Improves asthma control
Reduces emergency contacts with GP
Reduces hospital admissions
All should see an asthma nurse regularly – window to see asthma control

36
Q

what is acute severe asthma

A
Medical emergency 
Features 
PEFR 33-50% 
Cant complete sentences in one breath
Respirations >25 breaths per min 
Pulse >100 beats per min
37
Q

what are life threatening features of asthma

A
PEFR <33%
SpO2 <92% (regardless of air or oxygen)
Silent chest, cyanosis or feeble resp effort 
Arrythmia or hypotension
Exhaustion, altered consciousness
38
Q

how can acute severe asthma be managed

A

Oxygen
Corticosteroids (prednisolone 40-60mgs orally)
Nebulised bronchodilators (sal + ipratropium bromide)
Poor response = MgSO4 or intravenous aminophylline
Exceptionally intubation and ventilation

39
Q

how can someone with acute severe asthma be discharged

A

Discharge medication for 24 hours
Inhaler technique checked and recorded
PEFR >75% and PEFR diurnal variability <25%
Treatment with oral and inhaled steroids in addition to bronchodilators
Own PEFR and written PAAP
Follow up GP in a few days and resp centre after a 4 weeks

40
Q

how can peak flow variability vary

A

over 20% across a day for adults and children if asthmatic

41
Q

what would be an asthmatic results to a direct bronchial challenge test with histamine or methacholine

A

PC20 of 8mg/ml or less

42
Q

Salbutamol is an adrenoreceptor agonist, which receptor does it activate?

A

B2 receptor

43
Q

Following salbutamol activation, which cellular second messenger systems are activated and how do they produce the brochorelaxant effect?

A
G protein 
More ATP to cAMP via adenylate cyclase 
To protein kinase A
IP3 receptor (dec Ca2+ release ER) and MLCK (decreased association with Ca2+ calmouldin complex) 
inhibit smooth muscle contraction
44
Q

Common side effects of salbutamol include?

A

Increase heart rate (B1 and B2 agonist)
Tremor (B2 receptors)
Not used in diabetics as can affect beta cell

45
Q

what other conditions can salbutamol be used to treat

A

COPD

46
Q

how do smooth muscles constrict

A
methacholine>Muscarinic M3 receptor or histamine>Histamine H1 receptor activate G protein
Activate PLC (PIP2>IP3) 
\+ DAG
IP3R>Ca2+ released ER>MLCK
Myosin<>P-Myosin
MCLP (dec, by PKC, facilitated by DAG)