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Diploma in Anaesthesia > Autonomic nervous system physiology > Flashcards

Autonomic nervous system physiology Flashcards

1
Q

How can the ANS be classified

A

AFFERENT (sensory afferents transmit information from visceral structures, chemical and mechanical data from chemoreceptors and baroreceptors)

EFFERENT (controls cardiac muscle, smooth muscle and glands): two antagonistic divisions.

  • SNS
  • PSNS
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2
Q

Which structures are not innervated by the parasympathetic nervous system

A

Although most organs are innervated by both sympathetic and parasympathetic nerves, some-including the:

  • adrenal medulla,
  • arrector pili muscles,
  • sweat glands, and
  • most blood vessels-receive ONLY sympathetic innervation.
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3
Q

Where are the cell bodies for the pre-ganglionic ANS neurons found?

A

Brain or spinal cord

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4
Q

What type of axons are in preganglionic ANS neurons

A

B type fibres (diameter 2 um) velocity 10 m/s

myelinated but slow conducting

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5
Q

How many postganglionic cells does 1 pre-ganglionic cell synapse with?

A

8 - 9 –> diffuse ANS effect

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6
Q

What type of axons are in postganglionic ANS neruons

A

C-fibres (diameter 1 um), velocity 1m/s

un-myelinated and slow

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7
Q

From which spinal roots do the SNS preganglionic fibers emerge?

A

Thoracolumbar: T1 to L2

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8
Q

Where are the pre-ganglionic cell bodies found?

A

Lateral horn (grey matter) of the spinal cord

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9
Q

Describe the three ways that pre-ganglionic SNS axons can terminate after leaving the spinal cord?

A
  1. Synapse in the paravertebral sympathetic chain = series of sympathetic ganglie found alongside the vertebral column from the base of the skull to the coccyx
  2. Some pass through the sympathetic chain to synapse on PERIPHERAL AUTONOMIC GANGLIA
    - Caeliac ganglion
    - Superior mesenteric ganglion
    - Inferior mesenteric ganglia
  3. Few preganglionic SNS neurons synapse directly on chromaffin cells in the medulla of the adrenal gland
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10
Q

Describe the outflow of the PSNS from the CNS

A

Craniosacral

Cranial nerves: 3,7,9,10
- cell bodies are in cranial nerve nuclei

Spinal nerve roots S2 - S4
- cell bodies are in the lateral horns of the sacral spinal cord

The conus medullaris is at L1

The SAH space and dural sheath (and hence subarachnoid space) end at S2. –> LP avoids damage to spinal cord.

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11
Q

Where are PSNS ganglia

A

Ganglia from the vagus and sacral efferents are usually diffusely located in the walls of the viscera they supply

Cranial nerves 3, 7, 9 that supply the head and neck synapse in four discrete intermediary ganglia

  1. Ciliary
  2. Sphenopalatine
  3. Submaxillary
  4. Otic
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12
Q

How does the thoracolumbar SNS supply the head and neck and the pelvis

A

Preganglionic fibres from the thoracolumbar region travel up (or down) the paravertebral chain into cervical or sacral sympathetic ganglia to synaps with their postganglionic neurons

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13
Q

Which somatic pain fibres travel with PSNS efferents

A

Pain fibres from the lungs and pelvis travel with PSNS efferents

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14
Q

Which somatic pain fibres travel with SNS efferents

A

Pain fibres from the heart and abdominal viscera

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15
Q

Why is cardiac pain often referred to the arm and neck

A

Pain from viscera is poorly localized and is often ‘referred’ to the corresponding somatic segment

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16
Q

What therapeutic outcomes can be achieved by blocking the sympathetic pathways?

A
  1. Treat SNS overactivity
  2. Sympathetically mediated pain
  3. Visceral pain
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17
Q

Suggest clinical uses for the following sympathetic blocks:
Thoracic sympathectomy
Lumbar sympathectomy
Coeliac plexus block

A

Thoracic sympathectomy
- Raynauds phenomenon or hyperhidrosis (sweaty palms)

Lumbar sympathectomy
- Rx pain associated with circulatory insufficiency of the lower limb or phantom limb pain

Coeliac plexus block
- Rx pain associated with upper GI malignancy or acute/chronic pancreatitis

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18
Q

Which SNS postganglionic fibres use Ach instead of NA as a neurotransmitter

A

Merocrine sweat glands

Skeletal muscle blood vessels

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19
Q

Summarize the general properties of muscarinic receptors

A
  1. M1 - M5
  2. G-protein linked
  3. Brain, Heart, Smooth muscle, glands
  4. Actions are mimicked by muscarine (amanita mushroom)
  5. Actions are blocked by atropine
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20
Q

Summarize the general properties of the nicotinic receptors

A
  1. Found in ANS ganglia, the neuromuscular junction and merocrine sweat glands
  2. Ligand-gated ion channel receptors
  3. Mimicked by nicotine
  4. UNAFFECTED BY ATROPINE
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21
Q

When reversing non-depolarizing neuromuscular blockade, what classes of agent are given and why? What are the potential side effects and describe the mechanism of this and how it is prevented

A

Achase inhibitor (neostigmine) –> increase Ach within synaptic cleft –> competes with binding of non-depolarizing neuromuscular blocker.

The desired effect is to increase the Ach in the synaptic cleft in skeletal muscle to regain muscle function. But Ach is also increased at Muscarinic receptors since Achase is inhibited here too.

A Muscarinic blocking agent (Atropine or glycopyrrolate) is administered to prevent these unwanted muscarinic effects.

22
Q

How are alpha 1, Beta 1 and beta 2 receptors different from alpha 2 receptors

A

The former are all post-synaptic receptors whilst alpha 2 can either be a pre-synaptic or post-synaptic receptor

23
Q

How does noradrenalin and adrenalin affinity for alpha and beta receptors differ

A

Adrenalin ha a higher affinity for beta receptors

Noradrenalin has a higher affinity for alpha receptors

24
Q

Describe the G-protein linked mechanism for each type of adrenoreceptor and state how this brings about its function.

A

Beta

Linked to Gs protein: Ligand binding –> GDP converted to GTP on alpha subunit of the seven transmembrane protein. alpha-GTP detach and activate Adenyl cyclase –> converts ATP to cyclic AMP (cAMP) increased intracellular cAMP –> Contraction of cardiac muscle/Smooth muscle relaxation/glycogenolysis depending on location and B1 or B2.

alpha 2

Linked to Gi protein: inhibits the above process.

alpha 1

Linked to a Gq protein: Ligand binding –> GDP –> GTP: alpha subunit of G-protein bound to GTP detach –> activate Phospholipase C–> 1. activates IP3 (Inositol Triphosphate) –> mediates Ca2+ release and 2. activates Diacyl Glycerol (DAG) which activates protein kinases –> both 1. and 2. lead to smooth muscle contraction and glycogenolysis

25
Q

What types of adrenergic receptors are in the heart

A

Beta 1

26
Q

In arterioles and veins (Coronary, skeletal muscle ) what types of adrenergic receptors exist and what is the effect of their activation?

A

Beta 2 –> Dilatation

alpha 1 –> constriction

27
Q

Where are alpha 2 receptors found, what are their effects at these locations and give examples of alpha 2 receptor agonists

A

The role of the alpha(2)-AR family has long been known to include:

  • presynaptic inhibition of neurotransmitter release,
  • diminished sympathetic efferent traffic,
  • vasodilation (pre-synaptic) and vasoconstriction (post-synaptic).

Clonidine is an alpha 2 receptor agonist

Indications for clonidine: epidural infusion form in cancer pain not controlled by opioid analgesics and as an adjunct in anesthesia

28
Q

Which adrenergic receptors in the lungs lead to bronchodilatation?

A

B2

29
Q

Which adrenergic receptors in the lungs inhibit secretion from glands when stimulated

A

a1

30
Q

Which adrenergic receptors in the GIT decrease motility of the intestine when stimulated

A

a1, a2, B2

31
Q

Which adrenergic receptors in the intestine cause constriction of intestinal sphincters when stimulated

A

a1, B2

32
Q

Which adrenergic receptors in the skin cause piloerection

A

a1

33
Q

Which receptor in the skin causes SNS mediated sweating

A

Muscarinic !

34
Q

What does atropine do to the pupil and why

A

M antagonist –> relaxation of the sphinter (PSNS) of the iris –> unopposed contraction of the radial muscle (SNS) –> mydriasis

35
Q

What effect does adrenalin have on the eye?

A

a1 agonist –> contraction of the radial muscle of the iris –> mydriasis

36
Q

What is the MOA of ephidrine

A

Combined a and B agonist (weak) plus stimulates endogenous noradrenalin release

37
Q

What is the MOA of Phenylephrine

A

a1 agonist

38
Q

What is the mechanism of action of clonidine and what are the clinical uses of this drug

A

a2 agonist in brain stem –> activates an inhibitory neuron –> decreases SNS outflow from CNS –> decreased SVR, Renal vasc. resistance, HR, BP

Epidural clonidine may produce pain relief at spinal pre-synaptic and postjunctional a2 adrenoreceptors

Clinical use:

  • hypertension (not initial choice)
  • ADHD (decreased distractibility prefrontal cortex)
  • Epidural pain management
  • Sedation ICU (transition from dexmedetomidine to clonidine)
39
Q

What is the mechanism of action of isoprenaline

A

Stimulates beta1- and beta2-receptors resulting in relaxation of bronchial, GI, and uterine smooth muscle, increased heart rate and contractility, vasodilation of peripheral vasculature

Beta receptors relax everything except the heart

40
Q

What is the mechanism of action of Phentolamine

A

a-blocker

41
Q

What is the mechanism of action of propranolol

A

Nonselective beta-adrenergic blocker (class II antiarrhythmic); competitively blocks response to beta1- and beta2-adrenergic stimulation which results in decreases in heart rate, myocardial contractility, blood pressure, and myocardial oxygen demand. Nonselective beta-adrenergic blockers (propranolol, nadolol) reduce portal pressure by producing splanchnic vasoconstriction (beta2 effect) thereby reducing portal blood flow.

42
Q

What is the mechanism of action of Metoprolol

A

Selective inhibitor of beta1-adrenergic receptors; competitively blocks beta1-receptors, with little or no effect on beta2-receptors

43
Q

What is the MOA of Labetalol

A

Blocks alpha1-, beta1-, and beta2-adrenergic receptor sites; elevated renins are reduced.

The ratios of alpha- to beta-blockade differ depending on the route of administration estimated to be 1:3 (oral) and 1:7 (IV) (Goa 1989).

44
Q

What is the mechanism of action of neostigmine

A

AChase inhibitor

45
Q

What are the side effects of neostigmine

A 
Salivation
Nausea
Gut spasms
Bronchoconstriction
Bronchorrhoea
Bradycardia
46
Q

What are the side effects of Atropine

A 
Dry mouth and dry secretions
Blurred vision and dilated pupils
Tachycardia
Pyrexia 
Confusion
Bronchodilation
47
Q

What are the three common undesirable side effects of propranolol?

A
  1. Cold hands and feet
  2. Wheeze
  3. Worsening of intermittent claudication

Side effects occur because propranolol is a non-selective beta blocker

48
Q

How does general anaesthesia affect the SNS

A

Reduction in SNS tone, fall in BP and inhibition of autonomic reflexes.

Surgical stimulation during light anaesthesia may be associated with SNS responses such as tachycardia, Increased BP and sweating

49
Q

What procedures in the operating theatre might elicit a vasovagal episode and how can this be treated

A

Laryngoscopy
Traction on the eye
Traction on the peritoneum
Cervical dilatation

50
Q

What is the effect of spinal block for caesarian section on blood pressure? How can this be treated

A

Sympathetic block from T4 - L2 causes widespread vasodilation, decreased SVR and decreased BP.

Rx: Co-load with isotonic balanced fluid solution and administration of phenylephrine

51
Q

Apart from the diffuse vasodilation associated with spinal anaesthesia due to SNS block from T4 - L2, what additional effect does HIGH SPINAL block have on the CVS?

A

More profound hypotension due to greater sympathetic block and bradycardia from loss of sympathetic supply to the heart (T1 - T4).

52
Q

Is block to T10 adequate for caesarian section?

A

No block to T4 is require to block afferents from the visceral peritoneum

Diploma in Anaesthesia (73 decks)

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