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Pharmacology > parasympathetic nervous system drugs > Flashcards

parasympathetic nervous system drugs Flashcards

1
Q

what type of receptors does the neuromuscular junction use?

A

nicotinic receptors?

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2
Q

what is the difference between the receptors used in the neuromuscular junction and the autonomic nervous system?

A

their sub-unit composition is different

nicotinic receptors of the autonomic nervous system: can be antagonised by hexamathenoium/tubocurarine

nicotinic receptors of the neuromuscular junction can be antagonised by decamethenoium/tubocurarine

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3
Q

what is the structure of a nicotinic receptor?

A

5 sub-unit / ionotropic receptors

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4
Q

what is the structure of a muscuranic receptor?

A

7 sub unit/ G -coupled proteins

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5
Q

what are the agonists of the musurinic receptors? and what are the anatagonists of the receptor?

A

agonists:

  • LOW dosages of Ach
  • muscuraine

antagonists:
-atropine

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6
Q

what are the agonists of nicotinic receptors? and what are the antagonists of the receptor?

A

agonists:

  • HIGH dosages of Ach
  • nicotine

antagonists:

  • tubocuranine
  • repeated dosages of nicotine
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7
Q

what are some of the therapeutic uses of muscurinic agonists

A

relief of xerostoma (dry mouth) - pilocarpine
reduction of intra-ocular pressure (by constricting pupil) - pilocarpine
relief of urinary retention - especially if retention is caused by failure of reflex pathway - bethanechol

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8
Q

what are the effects of the muscuranic antagonists on the CNS?

A

anti-emetic (hyoscine)
reduces the intention tremor in PD (atropine)
in high dosages atropine causes marked stimulation: with restlessness, disorentation, hallucinations and confusion and thus can lead to cognitive impairment in the elderly

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9
Q

what are the effects of the muscuranic antagonists on the eye?

A

cause pupil dilation - for retinal examinations
cause paralysis of accommodation, allows lens to heal post operation

tropicamide: usually the short lived muscuranic antagonist used in the cases of eye examinations

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10
Q

what are some of the therapeutic uses of the muscuranic antagonists?

A

anti-emetics (powerful CNS depressant, causing sleep and amnesia) hyoscine

eye examinations: tropicamide

treatment of anti cholinesterase poisoning

symptomatic relief of SM spasm in asthma: ipratropium

anaesthesia (as pre-medication)
to reduce effects of vagal stimulation and anti-cholinesterase given during GI surgery
hyoscine/scopolamine

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11
Q

what are the side effects of muscuraninc antagonists

A 
reduced secretion 
reduced sweating 
reduction in tear production 
reduction in bronchial secretion 
urinary retention 
smooth muscle relaxation in the bronchus and bladder 
increase in heart rate, with no affect on blood vessels 
reduced GI motility and secretion
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12
Q

what are the effects of the muscurinic receptors in the heart?

A

they reduce heart rate, but have no negative ionotropic effect

the PS only spreads to the atria’s SAN and AVN
the M receptors slow the depolarisation of PM, meaning it takes longer for a threshold potential to be reached in order to generate an AP

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13
Q

why is the muscuranic agonist Ach not used clinically?

A

it is degraded too quickly by Che

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14
Q

what are the characteristics of the muscuranic agonists methacholine and carbacol?

A 
have a long duration of action 
they're quaternary amines
they're fully ionised 
no readily absorbed if given orally
not readily absorbed if given through the conjunctiva
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15
Q

what are the characterstics of the muscuranic agonist pilocarpine?

A

long duration of action
partially ionised at physiological pH
absorbed topically

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16
Q

what are the main side effects of muscuranic agonists

A

bardycardia (Reducing BP and CO)
vasodilation
salivation, lacrimation and sweating
bronchoconstriction and increased bronchosecretion
contraction of bladder detrusor muscle
increased GI motility
miosis and accommodation of the eye (reducing intra-ocular pressure)

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17
Q

what is the characteristic feature of the muscuranic antagonists?

A

they’re all tertiary bases - therefore, easily cross into the brain

quaternary derivatives are used to minimise CNS effects, but those are less selective peripherally

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18
Q

give two specialisations of the NMJ

A

pre-synpatically: vesicles containing high concentration of Ach are located at the active zone

post-synpatically: the membrane is thrown into folds, increasing the surface area of the post-synaptic cell

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19
Q

Hemicholinium acts on the NMJ, how?

where is most effective? when is its affect seen?

A

it inhibits choline uptake into the pre-synpatic terminal, through competitive antagonism to the choline carrier.

the choline carrier has a higher affinity for hemicholinium than choline

it is more effective at highly active synapses. its effect is not seen immediately but post-synaptic response gradually decreases

20
Q

name three drugs inhibiting acetylcholine release at the NMJ

A

botilinum toxin
tentanus toxin
aminoglycosides (hence they have a side effect of muscle weakness)

21
Q

name three competitive antagonists to the acetylcholine receptor at the NMJ

A

tubocuranine
gallamine
pancuronium

22
Q

explain how suxamethonium work

A

depolarising drug - blocks nerve transmission at the post-synpatic terminal

23
Q

what are the CNS effects of nicotine?

A

they increase both sympathetic and parasympathetic outflow
this causes:
- tachycardia
- increase in BP
- reduced gastric motility
- increased salivation and bronchial secretion
- increased ADH release

24
Q

what are the effects of ganglionic blocking drugs?

A

they indiscriminately block sympathetic and parasympathetic nervous system

CV effects: due to sympathetic blockage
- vasodilation and venodilation, huge reduction in BP
- loss of cardiovascular reflexes
GI tract effects: due to parasympathetic blockage
- inhibition of motility leading to severe constipation

genito-urinary tract: due to blockage of parasympathetic nervous system

  • microturition
  • failure of erection
  • failure of ejaculation (this is sympathetic mediated)

eyes: parasympathetic
- dilated pupils and loss of pupillary reflex (photophobia)
- loss of accommodation reflex (blurred vision)

25
Q

explain what a competitive neuromuscular block is? and give some of its feature?

A
  • it prevents Ach binding to AchR

features:

  • no fasiculuation
  • no post operative pain
  • no effect on the eye
  • hypotensive
  • increased effect in mysthania gravis
  • effect can be reversed with anti ChE
  • no change in plasma potassium concentration
26
Q

explain what a non-competitive muscular block is? and give some of its features

A
  • it depolarises the post-synpatic membrane, preventing the generation of an AP
  • acts on end plate region, making the cell inexcitable

features:

  • fasciculation
  • post operative pain
  • increased I.OP
  • NO hypotension
  • reduced effect in mysthania gravis
  • effect cannot be reversed with anti - ChE (perhaps even increased)
  • an increase in plasma potassium concentration
27
Q

give examples of competitive drugs

A

tubocuranine
gallamine
pancuronium

28
Q

give examples of a depolarising drug

A

suxamethonium

29
Q

give the differences between butylcholinesterase and acetylcholine esterase

A

butylcholinesterase:

  • soluble enzyme
  • found in many tissues, liver and plasma
  • hydrolsyses drugs

acetylcholinesterase:

  • membrane bound enzyme
  • found at cholinergic synapses (also found in RBC)
  • only hydrolysizes acetylcholine and similar compounds
30
Q

what is the dibucaine number?

why is it important?

A

this refers to the sensitivity of the enzyme butylcholinesterase to the inhibitor dibucaine
normal sensitivity: 70-90%
heterozygeous mutation to gene: 50-70% (show no altered sensitivity to suxamethonium
homozygous mutation to gene: 10-20% increased sensitivity to the drug suxamethonium

blood test routinely carried out, because of its implication when using anaesthetics

31
Q

how does the enzyme cholinesterase work?

A

2 binding site:
anionic site:
esterac site (with OH serine)

acetylcholine binds to both sites, acetyl group binds to the OH of the serine group, this causes the release of choline

the acetylated OH is hydroylses, releasing acetic acid

hydrolysis is at the rate of 10^4 molecules per second

32
Q

how do short acting reversible anti ChE work?

A

example: edrophonium

drug has a quaternary ammonium group, acts to the anionic site of the enzyme

competitive antagonism

33
Q

how do long acting reversible anti- ChE work?

A

example: neostigimine

drug binds to the OH serine group of the enzyme, forming an ester bond
drug ALSO binds to the anionic site
the hydrolysis of the acetylated drug takes a while –
rate of hydrolysis is 0.1 molecules per minute

34
Q

how do non reversible anti-ChE work?

A

example: DYFLOS and DFP
- those are organophosphate compounds
- irreversibly bind to the serine OH
- recovery of the OH group requires the synthesis of a new enzyme

these drug do NOT have a quaternary group, so inhibit other enzyme containing serine OH apart from ChE

35
Q

What are the peripheral effects of anti Che

A

NMJ:

  • repeated firing at the junction
  • reversal of nerve transmission due to muscular block or mysathenia gravis
  • in high dosages Ach could build up, this would lead to a depolarising muscular block

parasympathetic effect:

  • pupil constriction
  • bronchoconstriction and secretion
  • increased motility
  • bradycardia
36
Q

what are the central effects of anti - ChE drugs?

A

excitatory –> agitation and convuslion –> respiratory depression

37
Q

what are the therapeutic uses of anti ChE?

A

glaucoma: physostigmine
- reduced intra-ocular pressure

myasthenia gravis: neostigimine and pyrdiostygimine

  • those are quaternary compounds, used to minimise central effects
  • atropine used in conjunction to reduce peripherial actions
  • those drugs enhance synaptic transmission at end plate

GI tract: neostigimine

reversal of neuromuscular block after analgesia

38
Q

how do organophosphates cause damage? how is their action reversed?

A

they’re anti ChE inhibitors
their toxic effects are mediated by causing demyleination leading to paralysis and sensory loss (probably due to interfering with myelin synthezing enzymes)

cholinesterase activators are used:

  • oxime group (pralidoxime)
  • they bind to anionic site, and they entice the release of the phosphate from the esteraic site
39
Q

give an example of a non selective N/M receptor agonist?

A

acetylcholine and carbachol

40
Q

when is carbachol used?

A

used as eye drops in the treatment of raise intra-ocular pressure

has a long half - life because not hydrolysed by chE

41
Q

give examples of selective M receptor agonists?

A

methacholine (quaternary amine)
pilocarpine (tertiary amine - absorbed topically- xerostermia and reduction in I.O.P)
bethanachol (urinary retention)

42
Q

when is tropamide used? why not homatropine?

A

druring eye examination to cause cycloplegia and pupil dilation. it is used because it is shorter acting

43
Q

what agents would you use to induce cycloplegia after surgery?

A

long acting muscuraninc antagonists

e.g. atropine or hyscocine (probably atropine because hyscocine induces more drowsiness)

44
Q

what’s the difference between atropine and hyscocine?

A

hyscocine is used to reduce nausea, it also induces far more drowsiness

45
Q

what are parasympathomimetic drugs?

A
  1. those which act directly on the AchR (muscarnic agonists)

2. those that inhibit cHE therefore prolong and enhance the action of released Ach at the synapse

46
Q

what happens to HR and BP when using muscarinic antagonists?

A

BP does not change

  • no inneveration to most BV through parasympathetic system
  • HR increases (particularly in young and fit, because their HR is under vagal control)

Pharmacology (17 decks)

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