Treating Asthma Flashcards
What is the pathophysiology of asthma?
It is a TH2 driven eosinophilic inflammation causing:
Mucosal oedema
Mucus plugging
Bronchoconstriction
This eventually leads to airway remodelling which causes bronchial hyper-responsiveness.
How is bronchial smooth muscle innervated by the autonomic nervous system?
Bronchodilation is mediated by B2 adrenoreceptors via sympathetics. B2 agonists can be given to stimulate bronchodilation
Bronchoconstriction is mediated by M3 receptors via parasympathetics. Anticholinergics can be given in asthma but excessive PNS stimulation is not cause so they dont have much effect.
Outline the 5 stages of asthma treatment
Step 1- consider low dose ICS
Step 2- give low dose ICS
Step 3a- add inhaled LABA with low dose ICS (combination inhaler)
Step 3b- increase ICS, consider adding LTRA, SR theophylline, LAMA.
Step 4- increase ICS up to high dose. Add LRTA, SR theophylline, beta agonist tablet, LAMA
Step 5-add oral CS.
Why is medicine adherence, inhaler technique and management of trigger factors important in managing asthma?
The pathophysiology of asthma is inflammation which needs to be controlled otherwise it will just keep getting worse and worse.
How do leukotriene receptor antagonists work?
Leukotriene release by mast cells and eosinophils can induce bronchoconstriction, mucus secretion and mucosal oedema and promote inflammatory cell recruitment. LRAs block this effect.
What are the two types of LABAs?
Fast onset- eg formoterol
Slow onset- eg salmeterol
How do SABAs work?
Why should they not be used frequently?
Eg salbutamol, terbutaline.
Used for symptom relief as they prevent excessive bronchoconstriction on exercise.
Should not be used frequently because they decrease asthma control by causing increased mast cell degranulation
What are the side effects of B2 agonists?
Tachycardia
Palpitations
SNS stimulation symptoms
What is the mechanism of action of methylxanthines?
What is an example?
Eg SR theophylline
Inhibits Phosphodiesterase which degrades cyclin nucleotide second messengers.
This has the effect of bronchodilation.
Also works by adenosine receptor antagonism so prevents histamine and leukotriene release from mast cells.
How do long acting anticholinergics work?
Eg tiotropium bromide
Has anti PNS effects eg less bronchoconstriction
But also causes things like anhedonia etc.
Licensed for COPD and severe asthma. Reduces exacerbations.
How do corticosteroids work in asthma?
Reduce airway inflammation by:
Decreasing bronchial hyper-responsiveness
Causing production of anti inflammatory messengers- annexin 1, MKP 1.
Stopping production of inflammatory mediators- eg cytokines, chemokines, COX2
How does the size of the inhaled particle vary with how much the drug is absorbed?
0.5 microns- too small- inhaled into alveoli and back out again
1-5 microns- most effective as they settle in small airways
10 microns- deposited in mouth and oropharynx.
How do we classify severe asthma?
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Pulse > 100bpm
RR> 25bpm
Peak flow 33-50% best
How do we classify life threatening asthma?
Hypotension, bradycardia, arrhythmia
PEF< 33% SPO2<92% PaO2<8KPa PaCO2>4.5KPa Silent chest Cyanosis Feeble respiratory effort Exhaustion, confusion, coma.
How do we treat acute severe asthma?
Oxygen high flow- aim to keep 94-98%
Nebulised salbutamol
Oral prednisolone- 40mg daily for 10-14 days
If not responding add nebulised ipratropium bromide
Consider IV aminophylline if no improvement
Refer to ICU
