adult asthma features Flashcards
defining features
increased responsiveness of trachea and bronchi to various stimuli
manifested by widespread narrowing of airways that changes in severity either spontaneously or as a result of therapy
airway inflammation is mediated by the immune system
symptoms of asthma
SOB Wheeze (check severity) cough (paroxysmal, usually dry), sputum is occasional chest tightness (pain) diurnal variability episodic atopy
signs of asthma
wheeze on auscultation eczema obstructed spirometry PEF changes response to treatment
epidemiology of asthma in children
10-15%m>f
epidemiology of asthma in adults
5-10%
f>m
how many deaths are caused by asthma each year
1000
2/3 are preventable
proven risk factors of asthma
genetic
occupation
smoking
genetic risk factor
atopy
strongest risk factor: personal, familial atopic tendency
maternal atopy is the main influencer (3x father)
2 groups of genetic associations: immune response genes (IL-4, IL-5, IgE); airway genes (ADAM33)
disease clustering in families may be linked to environmental exposure
define atopy
inherited tendency to IgE response to allergens
asthma, eczema, hayfever and food allergy
occupation risk factor
10-15% of adult onset asthma
interactions w/ smoking and atopy
high risk jobs: bakers, welders, lab workers w/ animals, working w/ shellfish etc.
smoking risk factor
maternal smoking during pregnancy: reduced FEV1, increased wheezy illness, increased airway responsiveness, increased asthma and severity
grandmother effect - epigenetic modification of oocytes
what is the grandmother effect
link between smoking and OR asthma age 5
mother smoked - 1.5
maternal grandmother smoked - 2.1
mother and maternal grandmother smoked - 2.6
possible risk factors of asthma
obesity diet reduced exposure to microbes indoor pollution environmental allergens
obesity risk factor
BMI +vely associated w/ asthma, wheezing, airway hyperreactivity
diet risk factor
reduced antioxidant, n-3 polyunsaturated FA, increased n-6 polyunsaturated FA, increased/decreased vit D has associations w/:
- reduced FEV1
- increased wheeze
- increased asthma
- reduced wheeze and asthma; increased oily fish consumption and butter
supplementation in established disease is ineffective
reduced exposure to microbes risk factor
includes microbial products (endotoxin, glucans, extra capsular polysaccharide)
children born on farms are less likely to develop asthma
microbial diversity appears to be important in reducing risk of asthma and allergy
indoor pollution (chemical household products) risk factor
volatile organic compounds
formaldehyde
fragrances
cleaners at increased risk (OR 1.97)
people who use sprays weekly: 1.49x more likely to be asthmatic
people who use sprays 4x/wk: 2.11x more likely to be asthmatic
mothers who use sprays during pregnancy: children increased asthma
environmental allergens risk factor
house dust mite cats grass pollen exposure doesn't initiate atopy/asthma factors associated w/ affluence increase the likelihood of sensitisation to local allergens
house dust mites
warm, humid houses europe and coastal australia 200x own weight in droppings allergen is a protease in droppings exposure - pillows and bed
cats
universal exposure to allergen
evidence to show exposure may be protective
once sensitised, exposure is a major problem
clinical aspects
try to differentiate from other causes of wheeze
- localised airway obstruction, inspiratory stridor, tumour, foreign body
- generalised airflow obstruction: asthma (reversible AFO), COPD (irreversible AFO), bronchiectasis, bronchiolitis, CF
clinical Hx
symptoms evidence of variable symptoms: triggers and diurnal variation/weekly variation (occupational)/annual variation (environmental) PMH drugs FMH - atopic disease SH
symptom triggers
exercise cold air smoke perfume URTIs pets tree and grass pollen food aspirin
past medical Hx
childhood asthma
bronchitis
eczema
hay fever
drugs Hx
current inhalers (check technique and compliance) beta blockers aspirin NSAIDs effects of previous drugs/inhalers
social Hx
smoking
pets
occupations
psychosocial aspects (stress)
examination
THERE IS NO SINGLE DIAGNOSTIC TEST FOR ASTHMA
examination is usually unhelpful in clinic
what are we looking for on clinical examination
breathlessness on exertion
hyper-expanded chest
polyphonic wheeze
what would suggest asthma is unlikely on examination
clubbing, cervical lymphadenopathy (lung cancer)
stridor (tumour/foreign body aspiration)
asymmetrical expansion
dull percussion note (lobar collapse, effusion)
crepitations (bronchiectasis, CF, LVF, alveolitis)
what are we looking for evidence for in the essential investigations
airflow obstruction
variability and/or reversibility of AFO
spirometry: FEV1 <80%, predicted w/ FEV1/FVC ratio <70%
- in asthma may be completely normal
what would we do if spirometry shows airflow obstruction
exclude COPD/emphysema
reversibility to bronchodilator
reversibility to oral corticosteroids
how would we exclude COPD/emphysema
lung volumes (He dilution) gas trapping (increased residual vol, increased TLC, RV/TLC >30% CO gas transfer: transfer of CO to Hb across alveoli, looking for tissue destruction
how to we check for reversibility to bronchodilator
baseline
15 mins post inhaled salbutamol
baseline
15 mins post neb salbutamol
look for significant reversibility (change in FEV1 >200ml and change in FEV1 >12% baseline
BUT: no bronchoconstriction/severe bronchoconstriction, no reversibility
how to we check for reversibility to oral corticosteroids
anti-inflammatory separates COPD from astham prednisoslone for 14 days peak flow chart and meter baseline and 2wk spirometry
what do we do if spirometry shows normal airflow
check variability of lung function - lung function in clinical is usually normal
peak flow meter and chart - 2x daily for 2wks
- look for morning/nocturnal dips, reduction over wks/days, variability >20%
bronchial provocation - Nitrous oxide
diagnosis of occupational asthma
work related symptoms working w/ recognised occupational sensitiser confirmation: serial peak flow readings - 2hrly best: 5 days minimum - 2 pairs of exposed/unexposed periods
check antibodies
bronchial challenge
+ve response to colophony
specialist investigations for asthma
airway responsiveness to metacholine/histamine/mannitol
- normal lungs won’t respond
exhaled NO
what 3 other investigations can also be useful
CXR: hyperinflation, hyperlucent (no effusion, collapse, opacities, interstitial changes)
skin prick test: total and specific IgE (atopic status)
FBC: eosinophilia (atopy)
assessment of acute severe asthma
subjective parameters, not reliable
looks at: ability to speak, HR, RR, PEF, O2 sat/ABG
moderate, severe, life threatening, near fatal
moderate asthma
increased symptoms, no features of severe able to speak complete sentences HR <110 RR <25 PEF 50-75% predicted/best SaO2 >92% (no need for ABG) PaO2 >8kPa
Severe asthma
any one of: unable to speak, unable to complete sentences HR >110 RR >25 PEF 33-50% predicted/best SaO2 >92% PaO2 >8kPa
Life threatening asthma
any one of:
grunting
impaired consciousness, confusion, exhaustion
HR >130 or bradycardia (also arrhythmia and hypotension)
hypoventilation, silent chest, poor resp effort
PEF <33% predicted/best
cyanosis, SaO2 <92%, PaO2 <8kPa
PaCO2 normal (4.6-6.0kPa)
near fatal asthma
increased PaCO2
not being offloaded well enough
need for mechanical ventilation
