Respiratory pharmacology Flashcards
How do nerves control air flow in the bronchus?
Airway SMC can constrict and reduce the size of the lumen
The smaller it is, the higher the airflow resistance-
Can also be thinned by mucous, fibrous deposits, foreign bodies, etc
How does the ANS control airway constriction-what transmitters are used where?
PSNS-constrict the airway-controlled via vagus nerve to lungs-release ACh to nACH in ganglia then ACh to mACh in the airways
SNS-dilate the airways using Adrenaline/Nor -Preganglionic -ACh released to the nACh on adrenal medulla => release of NorA/A/Dopamine-to B2 receptors on lungs
In which parts of the ANS is ACh found?
All SNS - In every ganglia-from Pre-ganglionic
And to post-ganglionic to sweat gland
and SNS to adrenal medulla
PSNS-all neurons (pre and post ganglionic)
(and to NMJ-not ANS)
What receptors does ACh activate?
Muscarinic and Nicotinic
Why is ACh effects transient?
acetycholine esterase in the synaptic cleft–destroys ACh very fast –metabolised in synapse
How can you avoid side effects of muscarinic antagonists?
Topical (local administration)-straight to lung
Increase polarity-cant leave into blood stream
make em more M3 specific (or to the target yoou want)
What are the side effects of muscarinic antagonist?
Hot as hell, dry as a bone, blind as a bat, mad as a hatter
Why arent anti-histamines good treatment for ashtma?
Eosinophils are main cells in ashtma-and anti-hitamines would help with that
but loads of other contriction factors contribute-and removing only histamines doesnt solve the crisis
What endogenous factors contribute to bronchoconstriction?
Leukotrienes, Histamine, bradykinin, Prostaglandins,
What is good advice to give to astmatic before exercise?
Take inhaler-or give long acting bronchodilator
warm ups before exercises
Why do NSAIDS exarcebate ashtma?
Stop COX from acting-causing AA accumulation-more likely to down leukotriene pathway which cause bronchoconstriction