S11.2 Pharmacology of Airway Control Flashcards
Outline the pathophysiology of asthma
TH2 cells release cytokines, these activate inflammatory cells e.g eosinophil. Causes a type 1 hypersensitivity reaction, leading to airway narrowing as smooth muscle contracts, mucus is produced.
What is the step 1 management for asthma?
For mild intermittent asthma; SABA
This relaxes smooth muscle and reverses bronchoconstriction.
E.g salbutamol, terbutaline.
What is the step 2 management for asthma?
Inhaled corticosteroids
They improve symptoms and lung function.
Mechanism: transactivation occurs which upregulates B2 receptors. Also transrepression occurs which inhibits production of inflammatory molecules.
E.g beclomethasone, prednisolone
What is the step 3 management for asthma?
Add on therapy: LABA
Improve asthma symptoms and lung function, slower onset of action so not for acute attack
E.g salmeterol. Also formoterol (fast onset, long duration).
What is the step 4 management for asthma?
Alternative add on therapies: High dose ICS Leukotriene Receptor Antagonists Methylxanthines Long acting anticholinergics (LAMAs)
Describe the features of Leukotriene Receptor Antagonists
E.g montelukast
Block the effect of cysteinyl leukotrienes in the airways (which usually cause bronchoconstriction and mucus secretion etc)
ADRs; angioedema, dry mouth
Describe the features of methylxanthines
E.g theophylline, aminophylline
Antagonise adenosine receptors, inhibit phosphodiesterase, increase cAMP.
ADRs; nausea, headache
Levels increased by CYP450 inhibitors
Describe the features of long acting anticholinergics (LAMAs)
E.g tiotropium bromide, ipratropium bromide.
Bind to M3 muscarinic receptor and block it’s action (prevent bronchoconstriction)
ADRs: dry mouth, urinary retention
What is the treatment for acute-severe asthma?
High flow O2, nebulised salbutamol, prednisolone.
If life threatening or no improvement, consider ipratropium bromide or aminophylline.