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MD2002 Arvin > Structure of the Autonomic NS > Flashcards

Structure of the Autonomic NS Flashcards

1
Q

Describe the path of information from the brain to visceral effectors in the Autonomic NS.

A

Visceral motor nuclei in hypothalamus –> neurons (pre-ganglionic) descending into spinal chord or brain stem –> In ganglion, synapse with other neurons (post-ganglionic) –> Neuron –> Post-ganglionic neuron synapses with visceral effectors

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2
Q

Where do pre-ganglionic fibers originate from ? Post-ganglionic fibers ?

A

Pre-ganglionic fibers: from the CNS

Post-ganglionic fibers: from autonomic ganglia

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3
Q

Where specifically do the pre-ganglionic fibers of the SNS originate from ? of the PSNS ?

A

SNS: Thoracolumbar
PSNS: Craniosacral

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4
Q

Where specifically do the post-ganglionic fibers of the SNS originate from ? of the PSNS ?

A

SNS: Paravertebral Chain Prevertebral Ganglia
PSNS: In or Near Target Organ

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5
Q

Which of SNS or PSNS is long pre-ganglionic and which is long post-ganglionic fibers ?

A

SNS: Short pre-ganglionic neuron and long post-ganglionic neuron

PSNS: Long pre-ganglionic neuron and short post-ganglionic neuron

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6
Q

Does the vagus nerve serve the SNS or PSNS ? What structures does it innervate ?

A

PSNS

Viscera of trunk

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7
Q

Which organs are innervated by SNS and which by the PSNS ?

A

Broadly the same organs (pupils, salivary glands, heart, lungs, small intestine)
BUT SNS also innervates adrenal glands, kidneys, liver, sweat glands, blood vessels and structures of body walls.

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8
Q

What is a sympathetic trunk ? Where do they originate from and where do they extent to ? How do these trunks fuse with each other ?

A

Paired bundle of nerve fibers
Run from the atlas to the coccyx.

Fuse with each other in impar ganglion opposite coccyx.

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9
Q

What structure does the inferior cervical ganglion fuse with ? Where exactly does this occur ?

A

T1 ganglion to form the Stellate Ganglion

Lies on the neck of the 1st rib

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10
Q

What is the sympathetic supply to organs in the head ?

A

Internal carotid plexus

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11
Q

What are the four possible routes for a pre-ganglionic nerve leaving the CNS ?

A
  1. Enters sympathetic ganglion higher up (SYNAPSES) then ascends (has effectors in head and neck).
  2. Enters sympathetic ganglion at same level (SYNAPSES), and passes back into spinal nerve into periphery (sweat glands, smooth muscle) OR Enters sympathetic ganglion at same level, (SYNAPSES) and leaves into its own little nerve to influence viscera at that same level.
  3. Enters sympathetic chain (WITHOUT SYNAPSING) then descend into sympathetic ganglion (SYNAPSES ) (e.g. in sacral region) then passes back into a spinal nerve and then head off down to lower limbs.
  4. Enters sympathetic chain (WITHOUT SYNAPSING) passes out the front of sympathetic chain (still as pre-ganglionic neuron) then head to pre-vertebral ganglia (through splachnic nerve) in the abdomen. (SYNAPSES) then heads out to influence the gut.
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12
Q

Describe the general path of an autonomic motor reflex. What is the point of autonomic reflex arcs ?

A
  1. Stimulus in an organ (e.g. distended blood vessel)
  2. Sensory afferent neuron synapses at interneuron at CNS
  3. Pre-ganglionic fiber synapses at autonomic ganglion (may be SNS or PSNS depending on response required)
  4. Post-ganglionic fiber affects organ

POINT IS: VISCERAL CONTROL

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13
Q

What is a visceral pain response ?

A

Response to some distension, spasm, chemical irritation, ischiaemia.

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14
Q

What is referred pain ? Why does it occur ?

A

Pain from an organ, but felt as somatic pain (e.g. heart stroke, feeling in jaw and shoulder).
Because afferent neuron from injured organ to CNS synapses at same place as neuron from somatic region where the referred pain is actually felt.

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15
Q

Which of SNS or PSNS is fight or flight and which is rest and digest ?

A

SNS: fight or flight
PSNS: rest and digest

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16
Q

What is the effect of the SNS and PSNS on the heart ?

A

PSNS: Decreased heart rate
SNS: Increased heart rate + Increase rate of contraction

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17
Q

What is the effect of the SNS and PSNS on the digestive tract ?

A

PSNS: Increased motility and secretion
SNS: Decreased motility and secretion

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18
Q

What is the effect of the SNS and PSNS on the lungs ?

A

PSNS: Bronchoconstriction
SNS: Bronchodilation

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19
Q

What is the effect of the SNS and PSNS on the urinary bladder ?

A

PSNS: Release of urine
SNS: Urinary retention

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20
Q

What is the effect of the SNS and PSNS on the pupil of the eye ?

A

PSNS: Constrict
SNS: Dilate

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21
Q

What is the effect of the SNS and PSNS on the male sexual organs ?

A

PSNS: Erection
SNS: Ejaculation

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22
Q

What is the effect of the SNS and PSNS on the blood vessels ?

A

PSNS: Mainly no effect
SNS: Vasoconstriction (mostly)

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23
Q

What is the effect of the SNS and PSNS on salivary glands ?

A

PSNS: Increase secretion
SNS: Increase secretion

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24
Q

What is the effect of the SNS and PSNS on sweat glands ?

A

PSNS: No effect
SNS: Increased secretions

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25
Q

What is the effect of the SNS and PSNS on liver ?

A

PSNS: No effect
SNS: Glycogenolysis and gluconogenesis

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26
Q

What is the effect of the SNS and PSNS on pilomotor activity ?

A

PSNS: No effect
SNS: Piloerection

27
Q

What is the one instance where PSNS affects blood vessels ?

A

PSNS stimulates erection

28
Q

Describe the main features of ANS innervation of the eye ?

A

SYMPATHETIC: Contraction of Pupillary dilator muscle, resulting in Mydriasis (dilation of pupil)

PARASYMPATHETIC: Contraction of Pupillary constrictor muscle, resulting in Miosis (contraction of pupil)

29
Q

Describe the role of the ANS when the urinary bladder is

  1. Filling
  2. Full
A
  1. When bladder filling, SYMPATHETIC control predominates
    - Relaxation of detrusor muscle
    - Contraction of internal sphincter muscle
  2. When bladder full, PARASYMPATHETIC control predominates
    - Contraction of detrusor muscle
    - Relaxation of internal sphincter muscle
30
Q

Give an example where the SNS and PSNS have:

  1. Opposing effects
  2. Complementing effects
  3. Same effect
A
  1. Opposing effects (increase heart rate and increased force of contraction vs decreased heart rate)
  2. Complementing effects (erection and ejaculation)
  3. Same effect (increasing salivary secretions)
31
Q

Describe the ends of ANS.

A

Chains with Varicosities (each one containing neurotransmitter).

32
Q

What is the main difference in the nerve fibers between autonomic and somatic NS ?

A

Autonomic is a 2 neuron system (pre- and post-ganglionic fibers)
Somatic neurons go straight from CNS to target organ

33
Q

What neurotransmitter(s) is/are used in the ganglion where pre- and post-ganglionic fibres synapse in the SNS and PSNS respectively ? Which type of channel is used in the aforementioned ganglion.

A

In both SNS and PSNS, pre-ganglionic fiber releases ACh which binds to nicotinic ACh receptor.

34
Q

What neurotransmitter(s) is/are by post-synaptic fibers in the PSNS ? Which type of channel is used for this neurotransmitter ?

A

PSNS post-ganglionic fibers release ACh as neurotransmittter, which binds to muscarinic ACh receptor.

35
Q

Generally, what neurotransmitter(s) is/are by post-synaptic fibers in the SNS ? Which type of channel is used for this neurotransmitter ?

A

Generally, SNS post-ganglionic fibers release noradrenaline, which binds to adinergic receptors.
Some release ACh

36
Q

What are some of the exceptions to the aforementioned rules concerning the physiology of the SNS.

A
  1. Sweat gland, which is very similar to rule of PSNS (post-ganglionic fiber releases ACh which binds to muscarinic receptor).
  2. Adrenal medulla, long pre-ganglionic neuron goes directly to adrenal medulla, without ganglion (stimulates release of adrenaline from the medulla)
37
Q

Where on the adrenal gland does the preganglionic sympathetic fibers synapse ?

A

On chromaffin cells in the adrenal medulla

38
Q

What happens as a result of the Sympathetic innervation of the adrenal gland ?

A

Chromaffin cells release adrenaline and noradrenaline into systemic circulation, resulting in widespread tissue response

39
Q

What are the relative percentages of adrenaline and noradrenaline released by Chromaffin cells upon stimulation by the SNS ?

A 
Adrenaline = ~80%
Noradrenaline = ~20%
40
Q

Which kind of synapse are nicotinic ACh receptors present in ?

A

Present in ganglionic to post-ganglionic ganglion + in neuromuscular junction

41
Q

What are some of the main differences between Nicotinic and Muscarinic receptors ? What is the main similarity ?

A

NICOTINIC:
-Ionotropic

MUSCARINIC:
-G-protein linked receptor (metabotropic)

BOTH ACTIVATED BY ACh!

42
Q

True or false: Tissues innervated by both branches of the ANS generally have a predominate tone.

If true, give an example of a tissue and its predominant tone.

A

True.

Heart - PSNS

43
Q

What are some side effects of anticholinesterases on the ANS ?

A 
Salivation
Lacrimation
Urination
Defecation
GI upset
Emesis

Bradycardia
Hypotension
Bronchoconstriction
Pupillary Constriction

44
Q

What are predominate locations of Nicotinic ACh receptors ?

A

Neuromuscular junction
Sympathetic preganglionic
Parasympathetic preganglionic

45
Q

What are predominate locations of Muscarinic ACh receptors ?

A

Parasympathetic post ganglionic
Sweat glands (sympathetic)
Vascular smooth muscle
Central nervous system

46
Q

What are some factors which can be used to differentiate nicotinic receptors from muscarinic receptors ?

A

Different agonists

47
Q

Identify some agonists of ACh receptors, and state how good of an agonist (from + to +++) it is to each of muscarinic and nicotinic receptors.
Put the selective agonists in capital letters.

A

Acetylcholine (Nicotinic: +++ Muscarinic: +++)
NICOTINE (Nicotinic: +++ Muscarinic: /)
MUSCARINE (Nicotinic: / Muscarinic: +++)
BETHANECHOL (Nicotinic: / Muscarinic: +++)
PILOCARPINE (Nicotinic: / Muscarinic: ++)

48
Q

Which of nicotinic or muscarinic ACh receptors will drugs that affect the synthesis, storage, release and termination of ACh affect ?

A

Drugs that affect the synthesis, storage, release and termination of ACh will affect BOTH RECEPTOR TYPES

49
Q

May drugs that affect ACh at the Sk. NMJ affect the ANS ?

A

Yes

50
Q

What is a way of classifying muscarinic receptors ?

A 
M1 (neural) 
M2 (cardiac) 
M3 (glandular/smooth muscle) 
M4 
M5
51
Q

State the following for the M1 receptors:

  • Main locations
  • Cellular response
  • Functional response
A

MAIN LOCATIONS

  • Autonomic ganglia
  • Glands: gastric, salivary, lacrimal, etc.

CELLULAR RESPONSE
↑ IP3, DAG

FUNCTIONAL RESPONSE
Gastric secretions

52
Q

State the following for the M2 receptors:

  • Main locations
  • Cellular response
  • Functional response
A

MAIN LOCATIONS
-Heart: atria

CELLULAR RESPONSE
↓ cAMP

FUNCTIONAL RESPONSE
Cardiac inhibition (i.e. decreased heart rate)
53
Q

State the following for the M3 receptors:

  • Main locations
  • Cellular response
  • Functional response
A

MAIN LOCATIONS

  • Exocrine glands: gastric, salivary, etc.
  • Smooth muscle: GI tract, eye, airways, bladder
  • Blood vessels: endothelium

CELLULAR RESPONSE
↑ IP3, DAG

FUNCTIONAL RESPONSE
Gastric, salivary secretion
GI smooth muscle contraction 
Ocular accommodation 
Vasodilation
54
Q

Are all muscarinic receptors found in the ANS ?

A

No:

  • M1, M2, M4 and M5 are also found in CNS
  • M3 is found on vascular endothelial and smooth muscle cells
55
Q

Are all muscarinic ACh receptors excitatory ?

A

No, some are excitatory whilst others are inhibitory

56
Q

What are some some Muscarinic ACh receptor agonists ? State the pharmacological properties, and clinical uses of each.

A

PILOCARPINE
-Pharmacological properties: Non-selective muscarinic agonist
-Clinical uses: Glaucoma (to decrease IOP)
Xerostomia (following head/neck radiotherapy, induces salivation)
Constriction of pupils (miosis)

BETHANECHOL

  • Pharmacological properties: Non-selective muscarinic agonist
  • Clinical uses: Bladder and gastrointestinal hypotonia (Increases tone of the gut )W
57
Q

Why is the use of agonists of muscarinic ACh receptors limited ?

A

Because of their side effects, including restricted heart rate, restricted airways.

58
Q

How is the selectivity of action of muscarinic agonists achieved ? I.e How may one limit the side effects resulting from the usage of agonists of muscarinic ACh receptors ?

A

Place of administration, method of administration, and the ionised state of the drug.

59
Q

Is it possible to design drugs specific enough to traget one specific sub type of muscarinic receptor ?

A

No

60
Q

What are some Muscarinic ACh receptor antagonists ?

A

Atropine, Glycopyrronium, Hyoscine hydrobromide, Hyoscine butylbromid, Ipratropium, Tropicamide

61
Q

Name the pharmacological properties and clinical uses of each of the named Muscarinic ACh receptor antagonists ?

A

ATROPINE

  • Pharamocological Properies: Non-selective antagonist, Well absorbed orally, CNS effects
  • Clinical Uses: Adjunct for anaesthesia, Anticholinesterase poisoning, Bradycardia / cardiac arrest

GLYCOPYRONNIUM
-Pharmacological Properties: Similar to atropine
Does not cross blood brain barrier
-Clinical Uses: Similar to atropine

HYOSCINE HYDROBROMIDE

  • Pharmacological Properties: Similar to atropine, CNS effects
  • Clinical Uses: Hypersalivation, Motion sickness

HYOSCINE BUTYLBROMIDE

  • Pharmacological Properties: Similar to atropine but poorly absorbed, Does not cross blood brain barrier
  • Clinical Uses: Gastrointestinal spasms

IPRATROPIUM

  • Pharmacological Properties: Delivered via inhaler or nebuliser, Does not cross blood brain barrier
  • Clinical Uses: Maintenance treatment of COPD

TROPICAMIDE

  • Pharmacological Properties: Similar to atropine but shorter acting
  • Clinical Uses: Ophthalmic use (mydriasis)
62
Q

Are more illnesses due to increased or reduced PSNS activity ?

A

More diseases due to ↑ acti vity

63
Q

Why is there little therapeutic use for agonists of muscarinic ACh receptors ?

A

Because very few diseases of ↓parasympathetic activity, more due to ↑ acti vity

64
Q

What is the problem of selectivity with antagonists of muscarinic ACh receptors ? How is this controlled ?

A

Few differentiate between subtypes effectively. As a result, widespread side effects.

Control by route of administration and distribution

MD2002 Arvin (110 decks)

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