Asthma Flashcards
when talking to a patient about their asthma, what are the important parts of about their stable asthma that you should ask?
when diagnosed
what is their symptoms and control
triggers
treatment
education (understanding)/inhaler technique/adherence
complications (admissions, ICU, exacerbations)
physiology (lung function)
self-management (action plan?)
what are the characteristic findings for asthma on tests?
spirometry demonstrating airflow obstruction
and bronchodilator reversibility (>12%; at least 200mL FEV1)
peak flow variability of >20% over a few days is typical of asthma, but is not as solid as spirometry
What is the change that is required on a bronchial hyper-responsiveness test?
what types of agents are there? list some
We need to see a 20% fall in FEV1
the agents can be broken into direct and indirect challenges
When interpreting these results: it is important to recognise that all of these agents cause responsiveness at high doses. The test is to find out who reacts at a lower dose.
- direct challenges = act directly on receptors
- histamine (H1 receptors)
- methacholine (muscarinic receptors) - indirect challenges via an intermediate pathway
- hypertonic saline
- mannitol
- exercise
- hyperventilation
what is the mechanism of action of terubtaline?
this is a SABA (weird huh)
it is a PRN turbuhaler
what have been the “proven” benefits of ICS in asthma?
these have been shown to reduce symptoms
reduce freq of exacerbations
improve lung function
what has been the benefit of LABAs?
these are symptom controllers
whilst formoterol is actually fast onset (1-3 minutes) it lasts up to 12 hours! (formoterol/budesonide = symbicort, and this fast onset of action is the rationale behind the SMART therapy)
salmeterol is the more established LABA with onset 15-20 minutes
microscopically, what are some of the changes that we see at the gas-transfer membrane with chronic asthma/airway remodelling?
we see a lot of inflammation with increased cellularity during inflamm
the lamina reticularis is thickened, and the basement membrane also thickened.
HOWEVER, DLCO is typically normal or increased in asthma, possibly because of increased vascular recruitment and possibly even neovascularisation.
what is the mechanism of action of chromoglycate?
these are mast cell stabilisers
how does montelukast work?
this is a tablet taken daily that is not PBS funded
leukotriene receptor antagonist
Montelukast is a CysLT1 antagonist; it blocks the action of leukotriene D4 (and secondary ligands LTC4 and LTE4) on the cysteinyl leukotriene receptor CysLT1 in the lungs and bronchial tubes by binding to it. This reduces the bronchoconstriction otherwise caused by the leukotriene and results in less inflammation
what is ABPA?
how to diagnose?
a hypersensitivity response to the fungus Aspergillus (most commonly Aspergillus fumigatus)
ABPA causes airway inflammation, leading to bronchiectasis—a condition marked by abnormal dilation of the airways. Left untreated, the immune system and fungal spores can damage sensitive lung tissues and lead to scarring.
it is usually treated with steroids and itraconazole
diagnosis is a bit tricky. check skin prick test to aspergillus. IgG precipitin can be used, but is not really perfect (mid range sens and spec)
what is Omalizumab?
(Xolair)
what is the PBS requirements?
this is an anti-IgE agent that mops up free IgE. This then leads to decreased activation of mast cells, and then decreased influx of eosinophils.
the PBS has a pretty hefty requirement.
- Must have proven severe asthma (FEV1 reversibility or hyperresponsiveness)
- must have evidence of atopy from skin prick testing or RAST
- must have elevated serum IgE
must have been on high dose ICS and LABA
must have been on oral pred for >6 weeks
must have had exacerbations whilst on max treatment
in Australia how do we score the severity of asthma attacks?
overall it can be broken into mild, moderate and severe
PEF for mild >75%
mod 50 - 75%
severe 120 = severe
how does theophylline work?
Like other methylated xanthine derivatives, theophylline is both a:
- competitive nonselective phosphodiesterase inhibitor, which raises intracellular cAMP, activates PKA, inhibits TNF-alpha and inhibits leukotriene synthesis, and reduces inflammation and innate immunity
- nonselective adenosine receptor antagonist, antagonizing A1, A2, and A3 receptors almost equally, which explains many of its cardiac effects
