pharmacology 5 - autonomic system Flashcards

0
Q

what does the autonomic nervous system control? examples?

A

it controls involuntary activities. (non-concious)

eg. CVS, resp, endocrine, Gi tract motility and secretions, repro and urogenital tract.

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1
Q

what does the autonomic nervous system consist of? (3)

A

1, sympathetic division

  1. parasympathetic division
  2. enteric nervous system.
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2
Q

explain the SNS? where do you find the cell bodies? axons synapse at 3 sites? most commonly?

A

find cell bodies from 1st thoracic to 3rd lumbar segments.
axons synapse:
-paravertebral (parallel to spine) - most common
-prevertabral (in thorax/abdomen)
-terminal (close to organ)

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3
Q

what are the neourotransmitters for the SNS? what kind of innervation does the SNS have compared to the PNS?

A

1, preganglionic = ACH at nicotinic receptors

  1. norepinephrine (NA) - postganglionic at adrenoreceptors released from the nerve.
  2. epinephrine - also postganglionic at adrenreceptors - released from adrenal medulla.

the SNS has a much more diffuse innervation then the PNS.

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4
Q

what could you describe the response of the SNS as? give examples of the actions?

A

FIGHT OR FLIGHT!!
- mydriasis (pupil dilation due to constrivction of the radial mm)
-positively chonotrophic (increased heart rate)
-positively inotrophic (increased force of contraction)
-positively dromotrophic (increased speed on conduction)
- may vasodilate or constrict depending on receptor (mainly constrict) increased peripheral resistance.
-bronchdilatin
reduced GI motility and secretions
-increase urinary sphincter tone (prvent urination)
-glycogenolysis and GNG - increase glucose available - energy!!

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5
Q

what are the characteristic of norepinephrine? precursor? what is the main route of re-uptake etc? what role do alpha adrenorepectors play?

A

precursor - tyrosine!! also dopamine involved. once made it is stored in nerve terminals until an action potential come along nerve.
it undergoes mainly re-uptake but also enzymatic degratation.
alpha and beta adrenoreceptors.

alpha 2 adrenoreceptor - negative feedback on nerve terminal!!

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6
Q

explain the re-uptake of norepinephrine? 2 enzymes? which more important?

A

2 enzymes:

  • MAO - monamine oxidase - breaks down to release tyrosine in nerve terminal \9\re-used)
  • COMT - catechol-o-methyl transferase - into non terminal tissue (not re-used).
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7
Q

What are the SNS receptors? what kind of receptor? which second messanger? what second messanger for each receptor?

A

they are alpha and beta adrenoreceptors. 1/2.
they are GPCR - 7 transmembrane domains and couple to a second messanger within the cell itself. set up a cascade to release calcium - cell actions.
alpha 1 - coupled to Gq . second messanger is PLC - IP3 - DAG (CA2+ FROM SR) AND PKC which opens up ca2+ channels allowing influx to the cell.
alpha 2 - couple to Gi and Go . inhibit CAMP. which inhibits calcium and activates k+ channels 9RMP more negative.
beta 1 - couple to Gs (stimulate) and cause increased CAMP. and PKA. - increased calcium. cause positive effects on heart.
beta 2 - couple to Gs or Gi. can stimulate or inhibit CAMP. cause vascular sm relax (increased CAMP) bronchddilate, stabilise resp mast cells (asthma)

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8
Q

explain alpha 1 adrenoreceptor action when NA binds? actions? second messanger?

A
coupled to Gq receptor. causes PLC - cascade - DAG, IP3. PKC, SR  - CA2+!!! 
causes vasoconstriction
positive on heart
stimukate and contract prostatic sm
increase peripheral resistance
urinary sphincter contract
mydriasis (dilate pupil?)
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9
Q

alpha 2 adrenoreceptors? properties? what do they mediate? if lowered camp what happens to vascular sm?

A

coupled to Gi and Go. inhibit CAMP! less ca2+ release. activate k+ channels so moves out of cell and hyperpolarised. less likely to fire AP. inhibit neurotransmitter relase to (negative feedback) cause vasoconstriction (less cAMP) mediate sedation and analgesia!! i
if myocardial CAMP - down = relax
up = contract.

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10
Q

beta 1 adreoreceptors. coupled to?

A

coupled to Gs. (stimulate) heart. increase CAMP. inotrophic, chonotrophic, dronotrophic

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11
Q

beta 2 adrenoreceptors? mediate to which receptor? can do either? good for what type of disease?

A

Gs and Gi. can inhibit or stimulate via CAMP. vasculr SM relaxation (increased camp) Gs.
BRONCHDILATE - Gs AND INCREASED CAMP.
stabilise mast cells resp - less likely to release histamine - asthma (b2 agonists)

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12
Q

PNS - outflow from where? synapse where? neurotransmittier? receptors?

A

craniosacral outflow! - ACH neurotransmittir. synapse near organs (much more localised effect than SNS) nicotinic receptors and presynaptic and muscarinic receptors are postsynaptic.

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13
Q

how is ACH removed from nerve terminal? precursor? what is CAT?

A

mainly enzymatic degradation. AChetylcholine esterase. choline precursor is taken back up and used again. CAT - choline acetyl transferase - synthesis of ACH.

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14
Q

How can you explain action of PNS? give examples of the actions of the PNS? CVS? gi tract? urinary? eye? resp?

A

REST AND DIGEST!!!

CVS - decreased heart stuff
vasodilation and induces NO release (causes vasodilation)

GI tract - increased motility and secretions.
Urinary tract - contract detrusor, urethral peristalsis, relax sphincters
Miosis - pupil constriction
Respiratory - bronchconstrict and less secretions.

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15
Q

PNS receptors? 2 nicotinic? 5 muscarinic? M2 DOES WHAT?

A

nicotinic - presynaptic (common with SNS) ligand gated ion channel. increases permeability to NA and K+ .
Nm and Nn.
Nm - skeltal muscle (somatic NS)
Nn - ganglia 9autonomic)

Muscarinic - postsynaptic.
GPCR’s. M1-M5.
even - negative on CAMP. open k+channel
odd - PLC coupled and increase CA2+.

eg. M2 RECEPTORS ON THE HEART - NEGATIVE!!