12.2 respiratory Flashcards
what is the pathophysiology of asthma and what is it driven by?
- mucosal oedema
- bronchoconstriction
- mucus plugging
it is Th2-driven/ eosinophilic inflammation
what are the components of asthma control?
- minimal symptoms
- no exacerbations
- no limit of physical activity
- normal lung function (FEV1)
name two short acting b2 agonists
salbutamol and terbutaline
what is the importance of salbutamol?
it is used for symptom relief through reversal of bronchoconstriction
predominant action is on airway smooth muscle
why should salbutamol only be used on an as required basis?
short acting b2 agonist should only be used on a as required basis as if used regularly, reduces asthma control
what is the relation between salbutamol use and mast cell degranulation?
potentially inhibit mast cell degranulation if used intermittently, but if used regularly mast cell degranulation in response to an allergen increases
name 2 long acting b2 agonists
formoterol
salmeterol
what is the mechanism of action of inhaled corticosteroids?
they prevent inflammation by eosinophils so you don’t get mucosal oedema, bronchoconstriction and mucus plugging.
they do this through
- transactivation of B2 receptors
- trans repression of inflammatory mediators
give examples of 3 inhaled corticosterioids
beclomethasone dipropionate
budesonide
fluticasone
what should you prescribe long acting b2 agonists with?
inhaled corticosteroids as long acting b2 agonists are not anti inflammatory on their own
what are leukotriene receptor antagonists mode of action?
LTC4 released by mast cells and eosinophils can induce bronchoconstriction, mucus secretion and mucosal oedema, and promote inflammatory cell recruitment.
LRA’s block the effect of cysteinyl leukotrienes in the airways at the CysLT1 receptor
what are the ADRs of leukotriene receptor antagonists?
angioedema dry mouth anaphylaxis arthralgia fever gastric disturbances nightmares
give 2 examples of leukotriene receptor antagonists
montelukast
zafirlukast
what are the mechanisms of action of methylxanthines?
antagonise adenosine receptors
= inhibit phosphodiesterase = increase cAMP
what are the weak points of use of methylxanthines?
- poorly efficacious
- narrow therapeutic window
- frequent ADRs e.g nausea, headache, reflux
- levels increased by cytochrome p450 inhibitors