asthma Flashcards
definition of asthma
Chronic inflammatory airway disease
characterized by variable reversible airway obstruction, airway hyper-responsiveness and bronchial inflammation.
aetiology of asthma
genetic
- +ve FH
- atopy - (tendency of T lymphocyte (Th2) cells to drive production of IgE on exposure to allergens)
- genetic heterogeneity
env
- house dust mite
- pollen
- pets (urinary protein/fur)
- cigarette smoke
- viral resp tract infection
- aspergillus fumigatus spores
- occupational allergens (isocyanates, epoxy resins)
pathology of early phase of asthma (1hr)
Exposure to inhaled allergens in a presensitized individual results in cross-linking of IgE on the mast cell surface and release of histamine, prostaglandin D2, leukotrienes and TNF-a. T
= these mediators induce smooth muscle contraction (bronchoconstriction), mucous hypersecretion, oedema and airway obstruction.
pathology of late phase of asthma (6-12hr)
Recruitment of eosinophils, basophils, neutrophil and Th2 lymphocytes and their products
= perpetuation of the inflammation and bronchial hyper-responsiveness.
structural cells involvement in asthma pathology
Structural cells (bronchial epithelial cells, fibroblasts, smooth muscle and vascular endothelial cells),
may also release cytokines, profibrogenic and proliferative growth factors, and contribute to the inflammation and altered function and proliferation of smooth muscle cells and fibroblasts (‘airway remodeling’).
3 factors that contribute to airway narrowing
increased mucus production
mucosal swelling/inflamm
bronchoconstriction
epidemiology of asthma
either young as part of the ‘atopic triad’
or in adolescence and teenagers
affects 10% children and 5% adults
prevalence increasing
men=women
acute asthma medical emergency 1000-2000 deaths/yr UK
presenting symptoms of asthma
wheeze - lower airway obstruction (terminal bronchioles)
tight chest
difficulty breathing
intermittent dysponoea
cough - often nocturnal
sputum
worse:
cold,
exercise,
dust, pollen, fur
emotion
infection
smoking and passive smoking
drugs - B blocker/NSAIDs
worse in morning - diurnal pattern - get peak flow diary
distrubed sleep - severe asthma
reduced exercise tolerance
acid reflux
atopic disease: eczema, hay fever, allergy, FH, uticaria, nasal polyps
pets, carpets, feather bedding, soft furnishings
if symptoms stop at weekends - job trigger - paint sprayers, food processors, welders, and animal handlers) - Ask the patient to measure their peak flow at intervals at work and at home (at the same time of day) to confirm this
days off school
signs of asthma
tachypnoea
use of accessory muscles
prolonged expiratory rate
audible wheeze
polyphonic wheeze
hyperinflated chest
hyperresonant percussion
reduced air entry
widespread
moderate asthma exacerbation
- Increasing symptoms
- PEF 50-75% best or predicted
- No features of severe asthma
signs in severe asthma attack
PEFR <50%
pulse >110/min
RR >25/min
inability to complete sentences
signs of life threatening asthma attack
PEFR <33%
cyanosis
PaO2<8kPa but PaCO2 normal SpO2<92%
silent chest
bradycardia, arrhythmia
hypotension
confusion
coma
exhaustion, feeble resp effort
sign of near fatal asthma attack
high PaCO2
and/or needing mechanical ventilation with over inflation pressures
investigations for acute asthma
peak flow
pulse ox
ABG - normal/low Ox, low CO2 - hyperventilation, if PaCO2 is normal or raised, transfer to high-dependency unit or ITU for ventilation, as this signifies failing respiratory effort
CXR - exclude ddx
FBC - high WCC if infective exacerbation
CRP
UE
blood and sputum cultures
investigations for chronic asthma
PEFR monitoring - diurnal of >20% on ≥3d a wk for 2wks.
pul func test (spirometry) - obstructive defect (low FEV1/FVC, high RV), improvement after B agonist
blood - eosinophilia, IgE level, aspergillus Ab tutre
skin prick test - identify allergens
CXR - hyperinflation
histamine or methacholine challenge
management of acute asthma
resus, O2 sats, ABG, PEFR
high flow ox
salbutamol - nebulised B2-agonist bronchodilator (5mg initially continuously, then 2-4hrly. Ipratropium (0,5mg qds)
steroid therapy (100–200 mg IV hydrocortisone, followed by 40 mg oral prednisolone for 5–7 days).
If no improvement: IV magnesium sulphate. Consider IV aminophylline infusion or IV salbutamol, or ipratropium
Monitor oxygen saturation, heart rate, and respiratory rate.
Summon anaesthetic help if patient is getting exhausted (PCO2 increasing)
treat underlying casue
AB if chest infection - purulent sputum, abnormal CXR, raised WCC, fever
Monitor electrolytes closely (bronchodilators and aminophyline reduce K+
May need ventilation in severe attacks. If not improving or patient tiring, involve ITU early.
when can you discharge - asthma
PEF>75% within 1h of initial treatment can be discharged if no other reason to admit. otherwise:
- when PEF >75% predicted, best diurnal variation <25%, inhaler technique checked, stable on discharge med for 24hr
patient owns a PEF meter and has steroid (oral and inhaled) and bronchodilator therapy.
Arrange follow-up. - GP in 2 days, resp clinic in 4wks
theory of chronic asthma stepwise therapy
start on step appropriate to symptoms then either up or down (if control good for >3mo) to control symptoms
treatment reviewed every 3-6mo
rescue courses of prednisolone can be delivered at any time
step 1 - chronic asthma therapy
Inhaled short-acting b2-agonist as needed. If used >1/day, or night symptoms move to Step 2.
step 2 - chronic asthma therapy
As Step 1 plus regular inhaled low-dose steroids (400 mcg/day) eg beclometasone 200–800mcg/day (or fluticasone, budesonide or mometasone)
step 3 chronic asthma management
As Step 2 plus inhaled long-acting b2-agonist (LABA) (eg salmeterol 50mcg/12h by inhaler).
If inadequate control with LABA, increase steroid dose (800 mcg/day).
If benefit from LABA but control still inadequate – continue LABA and ICS and consider trial of other therapy – Leukotrine receptor antagonists, theophylline or Long-acting muscarinic receptor antagonists
If no response to LABA, stop and increase steroid dose (800 mcg/day).
step 4 chronic asthma management
increase Inhaled steroid dose (2000 mcg/day),
add a fourth drug, e.g. leukotriene receptor antagonist, SR theophylline or modified release b2-agonist tablet.
Refer patient to specialist care – although specialist care is mentioned in step 4, this may be required earlier and is ALWAYS indicated if there has been a recent severe or life-threatening exacerbation. In these cases follow-up is recommended for at least one year!
step 5 chronic asthma management
Addition of regular oral steroids (prednisolone) once daily at lowest possible dose.
Maintain high-dose inhaled steroid 20000mg/day
Consider other treatments to minimize the use of oral steroids.
Refer for specialist care
advice for asthmatics
educate on inhaler technique
routine monitoring of peak flow (twice daily)
develop an individualised management plan, emphasis on avoidance of provoking factors
quit smoking
weight loss
self-management by altering their medication in the light of symptoms or PEF.
Give specific advice about what to do in an emergency; provide a written action plan.
Consider teaching relaxed breathing to avoid dysfunctional breathing
mechanism of B agonists
B2-adrenoceptor agonists
relax bronchial sm - raise in cAMP, act in minutes
Salbutamol is best given by inhalation (aerosol, powder, nebulizer), but may also be given PO or IV
SE: tachyarrhythmias, low K+, tremor, anxiety.
Long-acting inhaled B2-agonist (eg salmeterol, formoterol) can help nocturnal symptoms and reduce morning dips:
- alternative to increasing steroids when symptoms are uncontrolled
- SE as salbutamol, paradoxical bronchospasm
mechanism of corticosteroids
inhale to avoid systemic effects eg beclometasone via spacer (or powder), but may be given PO or IV.
act over days to reduce bronchial mucosal inflammation
rinse mouth after use to avoid oral candidiasis
Oral steroids are used acutely (high-dose, short courses, eg prednisolone 40mg/24h PO for 7d) and longer term in lower dose (eg 5–10mg/24h) if control is not optimal on inhalers.
mechanism of aminophylline
(Metabolized to theophylline)
inhibit phosphodiesterase = reduced bronchoconstriction by increased cAMP
prophylaxis, at night PO - prevent morning dipping
useful as an adjunct if inhaled therapy is inadequate
In acute severe asthma, it may be given IVI.
narrow therapeutic ratio, causing arrhythmias, GI upset, and fi ts in the toxic range.
- check levels, do ECG monitoring and check plasma levels after 24h if IV therapy is used.
mechanism of anticholinergics
ipratropium, tiotropium
reduce muscle spasm synergistically with B2 agonists
not recommended for chronic asthma
mechanism for cromoglicate
mast cell stabaliser
May be used as prophylaxis in mild and exercise-induced asthma (always inhaled), especially in children.
It may precipitate asthma
mechanism of leukotriene receptor atagonists
(Eg oral montelukast, zafi rlukast.)
Block the effects of cysteinyl leukotrienes in the airways by antagonizing the CystLT1
mechanism of anti-IgE monoclonal Ab
Omalizumab 36 may be of use in highly selected patients with persistent allergic asthma.
Given as a subcutaneous injection every 2–4 wks depending on dose.
Specialists prescribe only.
drugs used in acute asthma
Salbutamol (B2-agonist). SE: tachycardia, arrhythmias, tremor, low K+.
Hydrocortisone and prednisolone (steroid; reduces inflammation).
aminophylline
- less frequently, not routinely recommended in current BTS guidelines, but may be initiated by respiratory team or ICU
- inhibits phosphodiesterase; increase [cAMP]
- SE: raised pulse, arrhythmias, nausea, seizures. - monitor ECG
- Aim for plasma concentration of 10–20mcg/mL (55–110μmol/L). Serious tox icity (low BP arrhythmias, cardiac arrest) can occur at concentrations ≥25mcg/mL.
- Measure plasma K+: theophyllines may cause low K+.
- Don’t load patients already on oral preparations.
complications of asthma
growth retardation
chest wall deformity (pigeon chest)
recurrent infections
pneumothorax
resp failure
death
prognosis for asthma
Many children improve as they grow older. Adult-onset asthma is usually chronic.
why are quiet breath sounds a bad sign
- patient may have blocked off large areas of the lung and may be getting tired. If not acted on, respiratory arrest may ensue rapidly.
- You would expect to hear widespread wheeze in most asthmatics with active disease
- increased pulse and respiratory rate are an additional concern in the presence of a ‘silent’ chest
why is normal PaCO2 concerning in an asthma attack
- would expect it to be low
- if normal/high – fail to keep up and soon go into worse resp failure
effect of adding LABA and montelukast
- halve the rate of exacerbation and their effects are additive.
SE of long term oral steroids
- Cataracts
- Weight gain
- Candida
- Osteoporosis
- Dm
- some risk of these side effects in asthmatics requiring frequent ‘short’ courses of oral steroids for exacerbations, although this is rare
how do you avoid candidiasis in pts using inhaled steroids
spacer device, rinses their mouth out with water after using the inhaler or cleans their teeth.
Cleaning of teeth also provides a useful memory trigger to aid concordance as most inhaled steroid regimes are twice daily inhalations, and most people clean their teeth twice a day
when do you give AB in asthma
- not routine
- unless signs of a bacterial infection (purulent productive cough, fever, leukocytosis, raised CRP, chest x-ray signs).
- A positive sputum culture in the presence of consolidation on a chest x-ray would require antibiotic treatment.
what is sufficient asthma control
- No daytime symptoms
- No night time waking due to asthma
- No rescue med needed
- Ne exacerbations
- No limitations in daytime activity including exercise
- Normal lung function (FEV1 and/or PEF >80% predicted or best) with minimal side effects
In females established on inhaled corticosteroids (ICS) what advice should you give
o The most recent revision of the BTS/SIGN guidance suggest continuing with short acting beta-2 agonists and inhaled corticosteroids as normal during pregnancy.
o Oral steroids should still be used if needed for asthma exacerbations during pregnancy
o Women with asthma should be advised of the importance of good control of their asthma during pregnancy to avoid problems for both mother and baby.
