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notes to flashcards year 2 - LCRS1 > cholinoceptor antagonists > Flashcards

cholinoceptor antagonists Flashcards

1
Q

define affinity

A
  • ability to bind to a receptor

- both agonist and antagonist

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2
Q

define efficacy

A
  • ability to induce a biological response

- agonist only

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3
Q

where are nicotininc receptors present? so what are nicotininc receptor antagonists?

A
  • present at all autonomic ganglia

- so nicotininc receptor antagonists = ganglion blocking drugs

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4
Q

what can GBDs act to do?

A
  • antagonise the receptor
    and/or
  • physically block ion channel itself
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5
Q

what are use-dependent blocks?

A
  • the drug works best when the channel is open so more of the receptor is used, the more is blocked
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6
Q

what is incomplete blocking?

A
  • 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
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7
Q

describe what SNS and PNS do

A

SNS - fight and flight

PNS - rest and digest

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8
Q

what effect would you have if a GBD was given at rest?

A
  • inc. HR and bronchodilation

- PNS dominant at rest and GBD blocks this

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9
Q

what would be the CVS, SM and exocrine effects of GBDs?

A

CVS: hypotension (blood vessel vasoconstriction inhibited, kidney renin seretion inhibited)
SM: pupil dilation, dec. GI tone, bladder dysfunction, bronchodilation
Exocrine secretions: dec.

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10
Q

give 3 examples of GBDs

A
  • Hexamethonium
  • Trimetaphan
  • alpha-bungarotoxin
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11
Q

what is Hexamethonium? MoA?

A
  • 1st anti-hypertensive drug but used LOTS of side effects as very general
  • primarily an ion-channels blocker (so not a lot of affinity)
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12
Q

what is Trimetaphan? MoA?

A
  • used for when you want hypotension during surgery
  • IV admin
  • short acting
  • primarily receptor antagonist (so has affinity)
  • can antagonise and block nicotininc receptors
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13
Q

what is alpha-bungarotoxin? MoA?

A
  • GBD that is irreversible
  • drug binds mainly to somatic nicotininc receptors
  • examples before bind to autonomic NRs
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14
Q

what are muscarininc receptor antagonists?

A
  • mainly PNS antagonist as only muscarinic receptor in SNS is found in sweat glands
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15
Q

give 2 examples of MRAs

A
  • atropine

- hyoscine

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16
Q

what are the CNS effects of atropine and hyoscine?

A

Atropine:
- normal dose: little effect
- toxic dose: mild restlessness –> agitation
Hyoscine:
- normal: sedation, amnesia
- toxic: CNS depression or paradoxical CNS excitation

17
Q

what are the opthalmic effects of tropicamide?

A
  • used in exam of retina

- causes dilation/miosis

18
Q

how can MRAs be used for anaesthetic pre-medication?

A
  • 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)
19
Q

how can a hyoscine patch be used against motion sickness?

A
  • 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
20
Q

how can MRAs be used against Parkinson’s?

A
  • 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
21
Q

what resp effects does ipratropium bromide have?

A
  • asthma and COPD

- causes bronchodilation

22
Q

what is the structure of ipratropium bromide?

A
  • 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
23
Q

what GI disease can an MRA be used for?

A
  • treats IBS

- dec. GI tone and secretions

24
Q

what are the unwanted effects of MRAs?

A
  • 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
25
Q

what drugs would you administer for atropine poisoning?

A
  • a drug that enhances ACh activity (anti-cholinesterase) or inhibits atropine
    e.g.
    physostigmine - anticholinesterase
    Bethanechol - MRA
    Ecothiopate - irreversible anticholinesterase
26
Q

what is the MoA of Botulinum toxin?

A
  • botulinum binds to ACh vesicles and stops them docking with inner membrane
  • forms SNARE proteins

notes to flashcards year 2 - LCRS1 (58 decks)

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