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SfM > Autonomic pharma of NMJ > Flashcards

Autonomic pharma of NMJ Flashcards

1
Q

Which set of receptors are ionotropic?

A

Nicotinic receptors

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2
Q

How many nicotinic subtypes are there?

A

2

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3
Q

How many muscarininc substypes?

A

3

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4
Q

How many adreneric subtypes?

A

5

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5
Q

How is synaptic tranmission curtailed?

A

TRansmitter binds to presynaptic autoreceptors which inhibit release of more transmitter

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6
Q

How is neurotransmitter in the synaptic cleft dealt with?

A

usually uptake to neurons or glia (except Ach is broken down)

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7
Q

NAme 5 ways to inhibit the NMJ

A

Inhibit choline transporter
Block voltage gated Ca2+ channels
Block vesicle fusion (botulinim toxins)
Non-depolarising (competetive antagonist) nicotinic receptor blockers
Depolarising nicotinic receptor blockers (agonist that keeps ion channel open (brief twitch then paralysis))

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8
Q

2 ways to improve NMJ function

A

Prolong action potential (make Ca2+ potential longer by inhibitin entry of K+ in order to release more Ach)
Block acetylcholinesterse

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9
Q

Clinical applications of non-depolarising (comp antagonists) and depolarising (sticky agonists) nictotinic receptor blockers?

A

Nicotinic receptor blockers used for paralysis:

  • surgical procedures
  • electroconvulsive therapy
  • controlling tetanus spasms.
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10
Q

Clinical applications for blocking vesicle fusion

A

Botulinum toxin used:

  • treating muscle spasm
  • cosmetic
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11
Q

clinical application of anti-cholinesterases

A
  • treating myasthenic syndromes (e.g. myasthenia gravis)
  • Reversing action of non-depolarising blockers
  • Countering botulinim poisoning
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12
Q

Whats ganglionic transmission?

A

Transmission between preganglionic and postganglionic autonomic fibres

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13
Q

How can ganglionic transmission be blocked that NMJ transmission cant?

A

By blocking the Ach activated ion channel in the post-synaptic membrane

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14
Q

How to increase ganglionic tranmission?

A

artificially activate nicotinic receptors (e.g. using nicotine which works better at ganglions than NMJ)

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15
Q

Why is there little to no clincal applications of altering ganglionic transmission?

A

Drugs would modulate sympathetic, parasympathetic and some NMJ transmission so the massive side-effects make it not worth while.

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16
Q

How can post-ganglionic parasympathetic transmission be modulated that the NMJ cant?

A

Muscarinic antagonists and muscarinic agonists.

17
Q

Clinical applications of muscarinic antagonists

A

Blocks action of parasympathetic system so:

  • relaxes smooth muscle in airways/bladder
  • Reduces gut motility
  • dilates pupil etc
18
Q

Clinical applications of muscarinic agonists

A

Mimic effect of parasympathetic system so:

  • slows heart rate
  • constricts pupil
  • contracts smooth muscle in airway/bladder
19
Q

Muscarinic agonists in glaucoma (high intraoccular pressure) treatment

A

aqueous humour normally drains through trabecular network into schlemm canal
Muscarinic agonist contract ciliary muscle and contract sphincter muscle
These open trabecular network and increase drainage of aqueous humour.

20
Q

4 ways to block postganglionic sympathetic transmission

A
  • block enzymes producing the NA
  • Block transporter that fill NA vesicles
  • Use false transmitter to activate inhibitory presynaptic autoreceptors (alpha2)
  • block alpha/beta postsynaptic receptors
21
Q

What are the 3 steps in producing NA from tyrosine?

A

Tyrosine -> DOPA
DOPA -> Dopamine
Dopamine -> Noradrenaline

22
Q

What enzymes are used converting tyrosine to NA?

A

Tyrosine hydroxylase
DOPA decarboxylase
Dopamine hydroxylase

23
Q

What blocks tyrosine hydroxylase?

A

Alpha-methyl-tyrosine

24
Q

What blocks dopa decarboxylase?

A

carbidopa

25
Q

What blocks dopamine hydroxylase?

A

6-hydroxydopamine

26
Q

What is tyrosine converted to, by what and what blocks it?

A

Tyrosine -> DOPA using tyrosine hydroxylase which is blocked by alpha-methyl-tyrosine

27
Q

What is DOPA converted to, how and hows it blocked?

A

DOPA -> dopamine by dopa carboxylase which is blocked by carbidopa

28
Q

What is dopamine converted to, by what and what blocks it?

A

Dopamine -> noradrenaline by dopamine hydroxylase which is blocked by 6-hydroxydopamine

29
Q

How to improve postganglionic sympathetic transmission? (sympathomimetics)

A
  • Stimulate NA release
  • Inhibit uptake into neurones
  • Activate postsynaptic receptors
30
Q

Clinical aplications of alpha1 agonists

A

decongestants and to dilate pupil (mydriatics)

31
Q

Clinical applications of alpha2 agonists?

A

treat hypertension (stops vesicle packaging of NA)

32
Q

Clincal applications of Beta2 agonists?

A

Treats asthma (relaxes smooth muscle in airways causin dilation.)

33
Q

Clinical applications of Beta1 antagonists?

A

treating hypertension, angina, cardiac, arrhythmias and glaucoma.

SfM (35 decks)

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