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Asthma - Mechanisms - Coggle Diagram
Asthma - Mechanisms
Mechanisms of hyperresponsiveness
Increased smooth muscle contractility
Hyperplasia
Hypertrophy
Increased excitatory nerve activity
ACh acting on M3 receptors causing contraction
ACh acts at M2 receptors on parasympathetic nerve inhibiting ACh release (negative feedback)
Loss of feedback loop can lead to increased enhanced airway contraction
eNANC transmitters acting on neurokinin receptors
Decreased bronchodilator activity
Adrenaline acts on B-adrenoceptors on airway smooth muscle
Inflammation
Epithelial damage
Exposure of sensory nerves
Oedema
Decreased luminal diameter
Pathological features
Chronic inflammation of the airways
Variable airflow obstruction
Increase is airway response to stimuli
B-agonists
Short-acting
Isoprenaline
Non-selective B-agonist
Salbutamol
Long-acting
Salmeterol
Formoterol
Order of lipophilcity
Formoterol
(lowest) Salbutamol
(highest) Salmeterol
Phosphodiesterase (PDE) inhibitors
Theophylline
PDE breaks down cAMP
Inhibition of PDE leads to increased cAMP, causing bronchodilaton
Aminophylline
Less potent and shorter acting
Lung function testing
PEFR
Peak expiatory flow rate
FEV1
Forced expiatory volume in 1 sec
Muscarinic antagonists
Ipratropium
Quaternary ammonium compound
Poorly absorbed
Lack of CNS effects
Competitive antagonist
Can be overcome by increasing ACh
Tiotropium
Blocks M3 receptor but preserves negative feedback loop