asthma Flashcards
what is the Britsh thoracic society’s definition of asthma
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
how does WHO define asthma
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.
how is asthma diagnosed
Combo of clinical assessment, objective tests but symptoms can change
why is asthma important
315 million adults worldwide
340,000 deaths a year
what is the impact of asthma
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
what is the natural history of asthma
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
what are causes of airflow obstruction
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
how do normal airways compare to asthmatic airways
narrower due to widened epithelium and smooth muscle (constriction)
mucous plug
enlarged mucous glands
what is atopy
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
what is the pathophysiology of asthma
antigens activate immune system, causing an inflammatory cascade, bronchoconstriction and inflammation (chemokine recruiting mast cells and eosinophils)
what are the symptoms of asthma
Cough
Wheeze
Breathlessness
Chest tightness
Occurs in episodes with periods of no (or minimal symptoms)
Diurnal variability so worse at night or early morning
what medications can trigger asthma
aspirin
ibuprofen
beta blockers
what are triggering factors of asthma
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
how can asthma be diagnosed
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)
what asthma investigations are done by a gp
Peak flow monitoring twice a day for two weeks
Spirometry may show airflow obstruction – could be normal between attacks
what asthma investigations are done by a gp/hospital
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
what are tests of lung function
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)
how is PEFR monitoring done
best of 3
what is FeNO
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
How can asthma be managed long term, non pharmacologically
Smoking cessation
Weight reduction
Pollution (provoke or exacerbate but effects of allergens, smoking and infection more sig)
How can asthma be managed long term, pharmacologically
Control of disease (preventers)
Inhaled corticosteroids (ICS)
Key part of first line treatment (eg beclometasone, fluticasone, budesonide, ciclesonide)
what are Inhaled long acting beta 2 agonists (LABA)
Formoterol, salmeterol
In combo with ICS as add on if still symptomatic
Never a single agent treatment alone, ass with inc deaths
how can asthma be treated orally (long term)
Oral leukotriene antagonist montelukast
Oral theophyllines
In patients with chronically poorly controlled asthma, low dose long term oral steroids by hospital direction
what are Short acting beta agonists (SABA)
Short/immediate relief of symptoms (relievers)
Salbutamol, terbutaline as inhaler (Sal 100mcg) or nebuliser (high dose salbutamol 2.5mg driven by oxygen)
what is maintenance and reliever therapy (MART)
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
What are the BTS guidelines for asthma
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
what are the two different inhaler devices
DPIs and pMDIs
what are DPIs
dry powder inhalers
activated by inspiration by patient
powdered drug dispersed into particles by inspiration
53-59% effective when used correctly
what are pMDIs
pressurised metered dose inhalers
drug dissolved into propellant HFCs under pressure, valve system releases metered dose
23-43% effective without spacer, with 55-57%
how is inhaler to use decided
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
what are specialist treatment
for a small number of patients with difficult asthma Monoclonal antibodies (anti IgE injections omalizumab or anti IL5 treatment mepolizumab)
what are unintentional barriers to treatment adherence
Misunderstanding Poor inhaler technique Language Forgetfulness Stress
what are intentional barriers to treatment adherence
Concern about side effects
Denial
Cost
how can asthma basely managed
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
what does a PAAP do (personal asthma action plan)
Improves asthma control
Reduces emergency contacts with GP
Reduces hospital admissions
All should see an asthma nurse regularly – window to see asthma control
what is acute severe asthma
Medical emergency Features PEFR 33-50% Cant complete sentences in one breath Respirations >25 breaths per min Pulse >100 beats per min
what are life threatening features of asthma
PEFR <33% SpO2 <92% (regardless of air or oxygen) Silent chest, cyanosis or feeble resp effort Arrythmia or hypotension Exhaustion, altered consciousness
how can acute severe asthma be managed
Oxygen
Corticosteroids (prednisolone 40-60mgs orally)
Nebulised bronchodilators (sal + ipratropium bromide)
Poor response = MgSO4 or intravenous aminophylline
Exceptionally intubation and ventilation
how can someone with acute severe asthma be discharged
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
how can peak flow variability vary
over 20% across a day for adults and children if asthmatic
what would be an asthmatic results to a direct bronchial challenge test with histamine or methacholine
PC20 of 8mg/ml or less
Salbutamol is an adrenoreceptor agonist, which receptor does it activate?
B2 receptor
Following salbutamol activation, which cellular second messenger systems are activated and how do they produce the brochorelaxant effect?
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
Common side effects of salbutamol include?
Increase heart rate (B1 and B2 agonist)
Tremor (B2 receptors)
Not used in diabetics as can affect beta cell
what other conditions can salbutamol be used to treat
COPD
how do smooth muscles constrict
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)
