The ANS 2 Flashcards

1
Q

What are the basic steps in neurotransmission?

A

1) Uptake of precursors
2) Synthesis of transmitter
3) vesicle storage of transmitter
4) depolarisation by propagated action potential
5) depolarisation-dependant influx of Ca2+
6) exocytotic release of neurotransmitter
7) diffusion to post-synaptic membrane
8) interaction with post-synaptic receptor
9) inactivation of transmitter
10) degradation or re-uptake of transmitter
11) interaction with pre-synaptic receptors

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2
Q

What is the process of Acetylcholine synthesis in Cholinergic transmission?

A

Acetyl CoA + Choline = Acetylcholine and Coenzyme A

Uses enzyme choline acetyltransferase (CAT)

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3
Q

What is the process of ACh degradation after cholinergic transmission?

A

Acetylcholine = acetate + choline

Uses acetylcholinesterase enzyme (AChE)

It’s an extracellular enzyme that coats the synapse membrane

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4
Q

Give an example of a drug that works on nAChR’s at autonomic ganglia?

A

Trimethaphan is a ganglion-blocking drug uses in hypertensive emergencies to produce controlled hypotension in surgery.

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5
Q

Why don’t drugs work at the nAChR’s on both the autonomic ganglia and the neuromuscular junction?

A

As the nAChR’s differ in structure so the drugs can only be specific to one

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6
Q

How many subtypes of mAchR’s are there?

A

5

These are M1 to M5 this is why drug selectivity is important as the different receptors have different actions.

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7
Q

Give an example of a new drug that DOES display limited tissue selectivity (on mAcHR’s)

A

Tolterodine is an mACHR agonist and is used to treat “overactive bladder”

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8
Q

How can the actions of endogenously released Ach be enhanced?

A

By using AChE (acetylcholinesterase enzyme) inhibitors. For example, Pyridostigmine is use to treat myasthenia gravis and Donepezil is used to treat Alzheimer’s.

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9
Q

Why are cholinergic drugs only used very selectively/

A

As their lack of selectivity often causes unwanted side effects.
Eg a non-selective muscurinc ACh receptor agonist is likely to cause autonomic side effects like, low heart rate+output, increased bronchi-constriction +peristalsis, salivation + sweating

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10
Q

What is SLUDGE a mnemonic for?

A

Mnemonic for the pathological effects of a massive discharge from the parasympathetic nervous system

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11
Q

What are the symptoms of SLUDGE syndrome?

A
Salivation 
Lacrimation (tears, eye water)
Urination 
Defecation 
Gastrointestinal upset 
Emisis (vomiting)
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12
Q

When is SLUDGE syndrome eneocuntered?

A

Drug overdose
Ingestion of magic mush rooms
Exposure to organophophorus insecticides (parathion)
Nerve gases (sarin or Novichok)

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13
Q

How is SLUDGE syndrome caused?

A

One way may be by a substance covalently modifiying ACHE stoping the breakdown of Ach so receptors in parasympathetic system are constantly innervated.

Symptoms primary due to chronic stimulation f mAchR in organs/muscles innervated by parasympathetic nervous system.

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14
Q

How is sludge treated?

A

Atropine (blocks mAchR’s)
Pralidoxime (gets rid of bound agents, releasing AchE)
Other anti-cholinergic agents (break down the Ach)

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15
Q

Give some examples and clinical uses of mAChR agonists (activators).

A

Pilocarpine and Bethanechol are used to treat glaucoma and to stimulate bladder emptying

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16
Q

Give some examples and clinical uses of mAchR antagonists (de-activators/blockers)

A

Ipratropium and Tiotropium used to treat asthma and COPD.

Tolterodine, Darifenacin and Oxybutynin used for overactive bladder

17
Q

What neurotransmitter do the majority of post-ganglionic sympathetic neurones release?

A

Noradrenaline

18
Q

What are vascorities?

A

Highly branched atonal networks on post-ganglionic sympathetic neurones. They’re a specialised site for Ca2+ dependant noradrenaline release

19
Q

What happens in noradrenaline transmission following Ca2+ release?

A

NA diffuses across synaptic cleft and interacts with adrenorecepotrs on ports-synaptic membrane to initiate signaling.

Na intersects with post-synaptic adrenoceptors to regulate processes in the nerve terminal

20
Q

How is NA removed form the synaptic cleft?

A

By noradrenaline transporter proteins.
Two transporter mechanisms “uptake 1” and ‘uptake 2”.
“Uptake 1” is aa Na+ dependant, high affinity transporter
“Uptake 2” is a lower affinity, non-neural mechanism

Another route is that any Na not taken up by vesicles in the re-synaptic terminal is susceptible to metabolism by the 2 enzymes = MAO and COMTa

21
Q

Give an example of. B2-drenoceptor gonist used clinically nd explain why its selectivity is important?

A

Salbutamol is used in sthm to reverse/oppose bronchoconstriction.

Selectivity is important s it limits possible cardiovascular side effects (positive iontropic nd chronotropic actions)