cholinoceptor antagonists Flashcards
define affinity
- ability to bind to a receptor
- both agonist and antagonist
define efficacy
- ability to induce a biological response
- agonist only
where are nicotininc receptors present? so what are nicotininc receptor antagonists?
- present at all autonomic ganglia
- so nicotininc receptor antagonists = ganglion blocking drugs
what can GBDs act to do?
- antagonise the receptor
and/or - physically block ion channel itself
what are use-dependent blocks?
- the drug works best when the channel is open so more of the receptor is used, the more is blocked
what is incomplete blocking?
- ion-channel blockade is only partial
- some ions pass through
- some GBDs do NOT have affinity as some types DON’T bind to receptor, just block ion channel itself
describe what SNS and PNS do
SNS - fight and flight
PNS - rest and digest
what effect would you have if a GBD was given at rest?
- inc. HR and bronchodilation
- PNS dominant at rest and GBD blocks this
what would be the CVS, SM and exocrine effects of GBDs?
CVS: hypotension (blood vessel vasoconstriction inhibited, kidney renin seretion inhibited)
SM: pupil dilation, dec. GI tone, bladder dysfunction, bronchodilation
Exocrine secretions: dec.
give 3 examples of GBDs
- Hexamethonium
- Trimetaphan
- alpha-bungarotoxin
what is Hexamethonium? MoA?
- 1st anti-hypertensive drug but used LOTS of side effects as very general
- primarily an ion-channels blocker (so not a lot of affinity)
what is Trimetaphan? MoA?
- used for when you want hypotension during surgery
- IV admin
- short acting
- primarily receptor antagonist (so has affinity)
- can antagonise and block nicotininc receptors
what is alpha-bungarotoxin? MoA?
- GBD that is irreversible
- drug binds mainly to somatic nicotininc receptors
- examples before bind to autonomic NRs
what are muscarininc receptor antagonists?
- mainly PNS antagonist as only muscarinic receptor in SNS is found in sweat glands
give 2 examples of MRAs
- atropine
- hyoscine
what are the CNS effects of atropine and hyoscine?
Atropine:
- normal dose: little effect
- toxic dose: mild restlessness –> agitation
Hyoscine:
- normal: sedation, amnesia
- toxic: CNS depression or paradoxical CNS excitation
what are the opthalmic effects of tropicamide?
- used in exam of retina
- causes dilation/miosis
how can MRAs be used for anaesthetic pre-medication?
- MRAs block PNS
- so block bronchoconstriction (get bronchdilation)
- blocks watery secretions (more thick secretions dec. chance of aspirations)
- blocks dec. HR and contractility (protects heart from slowing effects of other drugs)
how can a hyoscine patch be used against motion sickness?
- inhibits muscarinic receptors in vomiting centre
- so the sensory mismatch (from a mismatch from what the eyes see and what the labyrinth reports in balance) cannot induce vomting
how can MRAs be used against Parkinson’s?
- Parkinson’s: substantia nigra neurones lost, these usually produce dopamine for striatum
- MRA dec. -ve inhibition on release of dopamine into striatum from another source
- dopamine can continue to be released into striatum
what resp effects does ipratropium bromide have?
- asthma and COPD
- causes bronchodilation
what is the structure of ipratropium bromide?
- similar molecular shape to atropine
- has an extra nitrogen-containing polar group attached
- this allows it to linger more in lungs as it cannot cross mucosa as easily as atropine would
what GI disease can an MRA be used for?
- treats IBS
- dec. GI tone and secretions
what are the unwanted effects of MRAs?
- hot as hell: dec. in sweating, thermoregulation defects
- dry as a bone: dec. secretions
- blind as a bat: cyclopegia
- mad as a hatter: CNS disturbance
