Asthma Flashcards
Intro
what, presents as, peak incidence
- Chronic inflammation of the airways - due to a type 1 hypersensitivity reaction after exposure to triggers
- Presents as REVERSIBLE AIRWAY OBSTRUCTION due to narrowing ariways
- More common in children
Aetiology
- GENETIC PREDISPOSITION - antigen exposure causes IgE production (atopy)
- ENVIRONMENTAL FACTORS - passive smoking increases exposure and hygeine hypothesis says cleaner envts cause IgE response to allergens
Causes
- allergens - pollen, pets, mould
- drugs causing wheeze - NSAIDs (aspirin), B-blockers, penicillin
- dust, fumes, vapour - smoking, perfume, air pollution
- cold air
- occupational agents - flour, paint
- viral infections - rhinovirus, RSV, parainfluenza
risk factors
- personal/family history of atopy
- antenatal factors - maternal smoking
- low birth weight
- not breastfed
- passive smoking in childhood
- obesity
- air pollution
- increased exposure to triggers
- respiratory infections in infancy
- hygeine hypothesis
pathophysiology
Type 1 hypersensitivity reaction
= allergens stimulate type 2 helper T cells to rpoduce cytokines
= causes inflammation of airways
= bronchial hyperresponsiveness and reversible bronchoconstriction
symptoms
- wheezing
- cough - worse at night, non-productive
- shortness of breath on exertion
- chest tightness
signs
- expiratory wheeze on auscultation
- reduced PEFR
complications
reversible airway remodelling
- hypertrophy of SMC and mucous glands
- oedema, scarring, fibrosis
airway narrowing
- V/Q mismatch
- reduced ventilation of affected alveoli
mild/moderate asthma can lead to
type 1 respiratory failure
low O2 and low CO2
where pt hyperventilates to blow off the excess CO2 (inc resp rate)
progression to severe asthma is noticed when
pt can’t complete sentences in one breath
life threatening asthma can lead to
type 2 respiratory failure
high CO2 and low O2
where more airways are narrowed so bronchoconstriction
asthma exacerbations can be measured by
PEFR of best/predicted value
grading severity of asthma exacerbations
MODERATE
- PEFR >50-75%
- RR < 25/min
- pulse < 110 bpm
- normal speech
- increasing symptoms but no features of acute severe asthma
ACUTE SEVERE (type 1 resp failure)
- PEFR 33-50%
- RR > 25/min
- low CO2 (inc resp rate, hyperventilating so blowing off CO2)
- pulse > 110 bpm
- inability to complete sentences in one breath
LIFE THREATENING (type 1 resp failure)
- PEFR < 33%
- O2 sats <92%
- normal CO2 (4.6-6kPa)
- low O2 (<8kPa)
- silent chest
- cyanosis
- feeble respiratory effort
- bradycardia, arrhythmia, hypotension
- exhaustion, confusion, coma
NEAR FATAL (type 2 resp failure)
- raised CO2 (no gas exchange as more bronchoconstriction)
- require mechanical ventilation with raised inflation pressures
treating different severities
ACUTE SEVERE ASTHMA
- oxygen
- B2 agonists
- M2 antagonist (lungs) eg. ipratropium - antimuscarinic
- corticosteroids eg. prednisolone
LIFE THREATENING/NEAR FATAL
- move to ITU
- maybe need mechanical ventilation