ANS Flashcards

1
Q

Where does the sympathetic divisions of the ANS arrise from?

A

Thorasic and Lumbar regions

  • cell bodies in lateral horn
  • synapse with post in paravertable chain
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2
Q

Where does the parasympathetic regions of the ANS arrise from?

A

Cravinal and Sacral regions of th evertebral column

- Ganglia lie close to target organs

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3
Q

What the the pre-ganglionic neurtransmitters?

A

Para- ACh

Sympa- ACh

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4
Q

What are the post ganglionic neurotransmitters?

A

Para- ACh

Sympa- Noradrenaline

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5
Q

What are the post ganglionic receptors for ACh?

A

Muscarinic receptors;

  • M1/2/3
  • QIQ

GPCRs

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6
Q

What are the post ganglionic receptors for noradrenaline?

A

Adrenoreceptors;

  • a1/a1/b1/b2
  • QISS
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7
Q

What sympathetic postganglions don’t use noradrenaline?

A

Sweat glands
Piloecector muscles

Use Ach on muscarinic

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8
Q

What is the parasympathetic effects on the heart?

A

M2 receptors:
SA node- Bradycardia
AV node- reduce conductance volicity

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9
Q

What are the sympathetic affects on the heart?

A

B1 receptors:
SA node- Tachycardia
Ventricles- Positive inotropy

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10
Q

What is the sympathetic actions on the arteries?

A

A1 receptors:
Arteriolar contraction/ venous contraction

B2 receptors:
Arteriolar relaxation in some vascular beds

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11
Q

What are the parasympathetic effects on the bronchiolar smooth muscle?

A

M3 receptors:

Bronchiolar contraction

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12
Q

What are the sympathetic effects on the bronchiolar smooth mucle?

A

B2 receptors:

Bronchiolar relaxation

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13
Q

What are the basic steps in neurotransmission?

A
1- uptake precoursers
2- synthesis of transmitter 
3-vesicular storage of transmitter 
4-degradation of transmitter 
5-depolarisation due to apot
6-depolarisation dependant ca influx
7-exocytotic relsease of transmitter 
8- diffusion to post memb 
9-interaction post memb receptors 
10-inactivation of transmitter 
11-re-uptake of transmitter 
12-interaction with pre receptors
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14
Q

How do Muscarinic cholinoreceptor agonists act?

A

Vary in selectivity and resistance to degradation by choline esterase

Major clinical use- Glaucoma

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15
Q

How do nicotinic cholinoceptor antagonists act?

A

May have a preferential ganglion or nm blocking action

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16
Q

How do muscarinc cholinoceptor antagonists act?

A

Little sensitivity to subtypes
Vary in peripheral vs central actions

Reduce parasympathetic activity

17
Q

What is ACh synthasied from?

A

Choline and CoA by choline acetyle transferase

18
Q

How do drugs intefere with cholinergic transmission?

A
  • Interactions woth Cholinoreceptors

- cholinesterase inhibitors (decreases the rate ACH degrated so prolongs time ACh in cleft)

19
Q

What is noradrenaline synthasised from?

A

Tyrosine within nerve terminal

Tyrosine Hydroxylase (rate limiting enzyme)

20
Q

How is adrenaline synthasised?

A

Due to phenylethanolamine N-methyltransferase in chromaffin cells of adrenal medulla.

21
Q

How is adrenergic (noradrenaline) transmission limited?

A

Uptake 1- high affinity system
-rapildly reducing amount of noradrenaline in cleft

Uptake 2- lower affinity system

  • if escapes the cleft
  • can be re-vesiculated or metabololised
22
Q

How do adrenoceptor agonists assert an effect?

A

Highly selective to receptor subtype

Affect relates to what receptor acting on
Eg A1/2 or B1/2

23
Q

How do adrenoceptor antagonists cause an effect?

A

Are normally just A or B selective

Appose the effect binding to the receptor normally causes

24
Q

How do uptake 1 inhibitors cause an effect?

A

Centerally exert actions

Noradrenaline remains in cleft longer so adrenic effects produced

25
Q

At what stages in neurotranmission do drugs normally act?

A
  • degradation of transmitter
  • interaction with post synaptic receptors
  • inactivation of transmitter
  • re-uptake of transmitter
  • interaction with pre-synaptic receptors