L14 - inhaled therapies Flashcards
Obstructive lung disease
show reduced FEV1/FVC ratio under 0.7
reduction in expiratory flow rate
Asthma age of onset
usually less than 30
COPD age of onset
usually 35+
Asthma smoking history
no clear aertiology
COPD smoking history
usually 10+ pack-years
Asthma sputum production
infrequent
COPD sputum production
common in chronic bronchitis
Asthma allergies
often in early onset
COPD allergies
1/3 of general population
Asthma disease course
stable with exacerbations
COPD disease course
progressive with exacerbations
Asthma spirometry
likely to normalise with treatment
COPD spirometry
may improve but never normal
Asthma symptoms
intermittent and variable
COPD symptons
persistent and variable
Asthma treatment response
responds well to therapy, especially corticosteroids
COPD treatment response
less responsive to therapy
atopic asthma
fungal allergy, common aeroallergens, occupations, pets exposures
Non-eosinophilic asthma
non-smoking non-eosinophilic, smoking-associated, obesity-related
COPD
incomplete reversible airways obstruction, usually with a background of smoking or other fume/dust exposures, variable in individual presentations/specific phenotypes
COPD phenotypes
emphysema vs. chronic bronchitis
frequent exacerbations of 2 or more years
eosinophilic.non-eosinophilic inflammation
Asthma and COPD
increasing recognition of coexistence of diseases aka ACOS
Inhaled therapies
targeting for specific airway locations, minimises adverse effects
Drug deposition dependent on…
particle size, device delivery, drug nature, flow rates, underlying disease and regional differences in lung ventilation
Bronchodilators
beta agonists and muscarinic receptors
short-acting bronchodilators open up constricted smooth muscle in both asthma and COPD, nebulisers for high dose therapy
B2 agonist mechanism
Stimulation of B2-adrenoreceptors results in activation of adenylate cyclase, increased intracellular cAMP and subsequent airway smooth muscle relaxation
B2 agonist adverse effects
rising cAMP may activate Na+/K+ exchange pump
tachycardia, hyperglycaemia, loss of insulin selectivity, increased liver glucose release
Long acting B2 agonists
valuable bronchodilators with possible anti-inflammatory actions
Long-acting anti-muscarinics
parasympathetic nervous system regulates airway tone, these block ACh action on the muscarinic receptors which leads to bronchodilator and reduced mucus secretion
COPD without exacerbations
bronchodilator is the mainstay of treatment, LABA/LAMA with SABA as needed
Corticosteroids mechanism of action
Steroids treat the processes that drive remodelling. airway smooth muscle proliferation, epithelial injury
inhibit inflammation and promote epithelial integrity
Inhaled corticosteroids
minimise systemic absorption, reduce side effects to mostly localised adverse effects, range of inhaled steroids with varying potency
ICS in asthma
prescribed to almost all sufferers
ICS/LAVA combinations are common and effetive
ICS in COPD
more controversial, reduces exacerbation frequency, may increase pneumonia frequency, may be useful in ACOS
Asthma-COPD overlap
common, variable airway obstruction but not completey reversible, smoke exposure and infections, more symptomatic with greater healthcare burden
Fundamentals of treatment
concordance with therapy is poor - supervised trials using inflammatory markers to monitor
inhaler eduction is key
device selection is vital
Treatment goals
most patients have poor control, aim to improve control, address important issues for patients, maximum symptom relief with minimal side effects
Immediate management
oxygen up to 60%, salbutamol nebulise,r prednisolone and magnesium or aminophylline IV
