8- PNS anatomy- ignore

Question 1

Somatic nervous system

NT?

Receptors?

Answer 1

NT = Ach

Receptor = musle type nAChR–> ionotropic

Question 2

Parasympathetic nervous system

NT?

Receptors?

Answer 2

preganglionic = ACh

postganglionic = ACh

postganglionic = neuronal type nAhR –> ionotropic

End organ = muscarinic cholinergic receptor (MRs) –> GPCR

Question 3

Sympathetic nervous system

NT?

Receptors

Answer 3

preganglionic = ACh

postganglionic = NE

Postganglionic = neuronal type nAchR –> ionotropic

End organ = alpha or beta adrenergic receptors –> GPCRs

Question 4

exceptions to sympathetic nervous system and why

Answer 4

1) Adrenal medulla
no pre or post (NT = ACh) (receptor = nAchR)
adrenal medulla then release Epi –> alpha and beta adrenergic

2) Sweat glands
postganglionic release ACh not NE that acts on MRs in glands

3) Renal vasculature
postganglionic release dopamine not NE that acts on dopamine on D1 receptor –> vasodilation

Question 5

Describe concept of ANS “tone”

Answer 5

Tone = which action predominates based on which nervous system has bigger effect

Question 6

Which type of nervous system is most active during normal activity?
Important effects?

Answer 6

Parasympathetic = rest and digest

1) decr HR, decr contractility
2) constrict bronchial smooth muscle
3) incr GI (incr motility, relax sphicter, incr secretions)
4) incr motility of GU system
5) incr salivation

Question 7

exception to parasympathetic tone effects?

how does it compensate?

Answer 7

blood vessels
smooth muscle not innerv by PNS so sympathetic predominates –> vessel constriction

compensate with other mech (NO, adenosine) to dilate

Question 8

Cholinergic vs. Adrenergic

NT synthesis

Answer 8

Cholinergic
Acetyl CoA + Choline – ChAT –> ACh
(rate limiting = uptake of choline from synpase via ChT)

Adrenergic
tyrosine –TH –> DOPA – L-AADC –> DA – DBH –> NE
(rate limiting = conversion of Tyr –> DOPA)

both in presynap neuron

Question 9

Cholinergic vs. Adrenergic

storage

Answer 9

Cholinergic
Ach uptake via vesicular ACh transporter and stored in presynap vesicles

Adrenergic
DA uptake into vesicles via VMAT then convert to NE

Question 10

Cholinergic vs. Adrenergic

release

Answer 10

Cholinergic
ACh released when vesicles fuse with presynap membrane

Adrenergic
NE released when vesicles fuse with postsynap membrane

Question 11

Cholinergic vs. Adrenergic

Interaction with receptors

Answer 11

Cholinergic
ACh interact nAChR or MR based on synapse

Adrenergic
NE interact with alpha and beta adrenergic on target organ

Question 12

Effects produced by muscarinic cholinergic agonists that are SIMILAR to stim of PNS

Answer 12

1) incr salivation
2) miosis and accomodation
3) incr urinary and GI motility

Question 13

Effects produced by muscarinic cholinergic agonists that are DIFFERENT to stim of PNS

Answer 13

1) vasodilation (decr peripheral resistance)

2) incr sweating with sympathetic cholinergic

Question 14

Contrast actions and use of bethanechol vs pilocarpine (both muscarinic cholinergic agonists)

Answer 14

Bethanechol = quaternary AA –> can’t cross BBB
fxn = oral to treat urinary retention and paralytic ileus (bowel blockage)
= long half life and resistant to metab by AChE

Pilocarpine = tertiary AA –> pass thru BBB
fxn = droplets to cause miosis in cataract surgery
= glaucoma
= dx deficient salivation (xerostomia)

Question 15

How does AChE inhibitors affect cholinergic neurotransmission
uses of reversible vs irreversible

Answer 15

incr ACh in synapse –> potentiate ACh on muscarinic and/or nicotinic receptors

reversible = therapeutics
irreversible = nerve gas and pesticides

Question 16

Names of AChE inhibitors

Answer 16

Physostigmine (3’ amine)
Donepizil (3’ amine)
Neostigmine (4’ amine)
Edrophonium (short acting 4’ amine)

Question 17

Uses of AChE inhibitors

Answer 17

1) Glaucoma
2) Alzheimer’s
3) urinary retention
4) paralytic ileus
5) myasthenia gravis

Question 18

Sx of organophosphate poisoning

Answer 18

irreversible inhibiton of AChE 
causes SLUDGE 
S = salivation/sweating
L = lacrimation
U = urinary retention
D = diarrhea
G = GI cramping and emesis
E = emesis

Question 19

organophosphate poisoning
Potentiation at nAChRs at NMJ leads to ___ then ___

Potentiation at AChR in CNS lead to __, ___, and ___

Answer 19

sustained muscle contraction, then depression

anxiety, convulsions, depression

Question 20

How to treat organophosphate poisoning

Answer 20

pralidoxime binds organophosphate and removes from AChE

Atrpine = cross BBB and block MR

Treat convulsions with diazepam

Question 21

Atropine and scopolamine are both ___

Answer 21

muscarinic cholinergic antagonist, incr ACh required to produce effect

Side efects

1) dry mouth
2) decr sweating
3) CNS stim
4) depression (scopolamine more)

Question 22

therapeutic uses of MR antagonists

atropine

Answer 22

atropine uses = mushroom poisoning, AChE inhibitor toxicity, bradycardia, asthma attk

Question 23

therapeutic uses of MR antagonists

scopolamine

Answer 23

preanesthetic, motion sickness

Question 24

therapeutic uses of MR antagonists

tropicamide

Answer 24

ophthamologic exams –> mydriasis and cycloplegia

Question 25

therapeutic uses of MR antagonists

other uses

Answer 25

urinary incontinence
COPD
asthma
rhinorrhea