asthma Flashcards
factors that regulate bronchial airway tone
sympathetic NS relaxation (beta-2)
parasympathetic NS contraction (M3)
Histamine contraction (H1)
leukotrienes inflammation (LT-1)
adenosine mast cell destabilization
cAMP relaxation
treatment of the acute symptoms (rescue) of asthma
beta agonist
anti-cholinergic
methylxanthine
treatment to prevent atacks (prophylactic/controller)
corticosteroids
anti-leukotrienes
plus rescue agent
intermittent attacks
<5 days/month
recurrent attacks
> 5 days/month
> 3 months/year or >50% of the days in any one month
short-acting b-adrenergic agonists
albuterol
terbutaline
pirbuterol
bitolterol
MOA and use of short-acting beta adrenergic agonists
(acute) to dilate bronchial smooth muscle
MOA: activation of b2-adrenergic receptors
long-acting b-adrenergic agonists
salmeterol
formoterol
MOA and use of long-acting b-adrenergic agonists
recommended as controller but can be used for acute
MOA: activation of b2-adrenergic receptors
methylxanthines
theophylline, theobromine, caffeine
MOA and use of methyxanthines
both controller and rescue
MOA: nonspecific inhibition of PDE inhibtion of adenosine receptors
difference between short and long-acting b- adrenergic agonists
short-acting = “as needed” for acute sx
long acting = prophylaxis (nocturnal); NOT RECOMMENDED for tx of acute sx due to beta-adrenergic receptor desensitization but can be used in emergency
similarity between short and long-acting b- adrenergic agonists
both produce bronchodilation
why are methylxanthines not used as often?
narrow therapeutic window
availability of newer, safer agents
actions of methylxanthines
at concentration can inhibit PDE4 to increase cAMP and cause bronchodilation
at low concentrations can at on A2A receptor to promote wakefulness via vasoconstriction of cerebral blood vessels
act on A2B to block adenosine-mediated mast cell degranulation