Autonomic nervous system Flashcards

1
Q

what are the anatomical divisions of the brain stem and spinal cord

A
medullary 
cranial
thoracic
lumbar
sacral
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2
Q

what anatomical divisions are part of the sympathetic

A

thoracic

lumber

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3
Q

which anatomical divisions are parasympathetic

A

medullary

sacral

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4
Q

parasympathetic nerves

A
  • originate in the lateral horn of the medulla and sacral spinal cord
  • have long myelinated preganglionic fibres
  • short postganglionic unmyelinated fibres
  • ganglia are located within the innervated tissues
  • have action sthat oppose the sympathic nervous system
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5
Q

sympathetic nerves

A
  • originate in the lateral horn of lumbar and thoracic
  • have short myelinated preganglionic fibres
  • have long unmyelinated postganglionic fibres
  • ganglia are located in the paraventerbral chain close to the spinal cord
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6
Q

What neurotransmitter do all pre-ganglionic neurons use?

A

they are cholinergic- Acetylcholine

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7
Q

what neurotransmitter do parasympathetic post-ganglionic neurons use?

A

cholinergic
ACh
muscarinic ACh receptors in the target effector tissue

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8
Q

what type of neurons are most of the post-ganglionic sympathetic nerves?

A

most are noradrenergic

-they use noradrenaline

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9
Q

what major class of adrenoceptors does Noradrenaline use

A

alpha-adrenoceptors and beta-adrenoceptors

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10
Q

which sympatheic post-ganglionic neurons are cholinergic not adrenergic

A
  • those innervating sweat glands, hair follicles- piloerection
  • they release ACh that acts at muscarinic ACh receptors
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11
Q

sympathetic postganglionic neurons in adrenal glands

A
  • are differentiated to form neurosecretory chromaffin cells
  • chromaffin cells can be considered as postganglionic sympathetic neurons that do not project to a larger tissue
  • instead, on sympathetic stimulation these cells release adrenaline into the bloodstream
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12
Q

What does parasympathetic release of ACh at M2 cause?

where are M2 adrenoceptors?

A

M2

  • bradycardia
  • reduced cardiac conduction velocity

heart

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13
Q

what are the most common sites for drug intervention in neurotransmission?

A
  • degradation of neurotransmitter
  • interaction with post-synaptic receptors
  • inactivation of transmitter
  • re-uptake of transmitter
  • interaction with pre-synaptic receptors
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14
Q

what enzyme breaks down acetylcholine

A

acetylcholinestase

AChE

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15
Q

what enzyme makes acetylcholine

A

choline acetyltransferase

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16
Q

what are the consequences of lack of selectivity of cholinergic drugs - muscarinic ACh receptor agonist

A

heart:
decreased heart rate and cardiac output

smooth muscle:
increased bronchoconstriction
increased GI peristalsis

exocrine:
increased sweating and salivation

17
Q

what is SLUDGE syndrome

A

the pathological effects indicative of massive discharge of the parasympathetic nervous system

Salivation
Lacrimation
Urination
Defecation
Gastrointestinal upset
Emesis
18
Q

what causes SLUDGE syndrome

A

drug overdose
ingestion of magic mushrooms
exposure to organophosphorus insecticides
exposure to nerve agents

prolonged over stimulation of muscarinic acetylcholine receptors

19
Q

termination of noradrenergic transmission

A

reuptake into the pre-synaptic terminal by a Na+-dependant, high affinity transporter

if not taken up by reuptake it is taken up by a lower affinity, non-neuronal mechanism

20
Q

what is the fate of NA not taken up into vesicles

A

it is susceptible to metabolism by 2 enxymes

  • monoamine oxidase
  • catechol-O-methyltransferase
21
Q

what opposes bronchoconstriction in asthma

A

beta-2 adrenoreceptor-selective-agonists- salbutamol

22
Q

basic steps in neurotransmission that can be common sites of drug action

A
  1. degradation of transmitter
  2. interaction with post-synaptic receptors
  3. inactivation of transmitter
  4. re-uptake of transmitter
  5. interaction with pre-synaptic receptors
23
Q

basic steps of neurotransmission

A
  1. uptake of precursors
  2. synthesis of transmitter (T)
  3. vesicular storage of transmitter
  4. degradation of transmitter
  5. depolarisation by propagated action potential
  6. influx of Ca2+ in response to depolarisation
  7. exocytotic release of transmitter
  8. diffusion to post-synaptic membrane
  9. interaction with post-synaptic receptors
  10. inactivation of transmitter
  11. re-uptake of transmitter or degradation product(s)
  12. interaction with pre-synaptic membrane
24
Q

What does parasympathetic release of ACh at M3 cause?

where are M3 adrenoceptors?

A

M3

  • bronchial contraction
  • increased intestinal mobility/secretion
  • bladder contraction and relaxation
  • penile erection
  • cillary muscle and iris sphincter contraction

smooth muscle

25
Q

What does parasympathetic release of ACh at M1/ M3 cause?

where are M1/M3 adrenoceptors?

A

M1/M3
-increased sweat/salivary/lacrimal secretion

glandular

26
Q

What does sympathetic release of noradrenaline cause at the b1? and where are b1 receptors

A

beta 1

  • tachycardia
  • positive inotropy and chronotropy

heart

27
Q

what does sympathetic release of noradrenaline do on smooth muscle?

A

arteriolar contraction/ venous contraction- a1 b2

bronchiolar/intestinal/uterine relaxation b2

28
Q

how do you treat sludge

A

treated with atropine, pralidoxine