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Primary FRCA > Physiology 14 > Flashcards

Physiology 14 Flashcards

1
Q

Where do preganglionic sympathetic fibres travel? What type are they?

A

Lateral cord - B fibres

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2
Q

Where do sympathetic preganglionic fibres synapse?

What type of fibres are the postganglionic neurones?

A

Sympathetic chain - C fibres

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3
Q

From where does the sympathetic supply to the head and neck arise?

A

Superior, middle and stellate ganglia

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4
Q

What is different about the autonomic supply to the adrenal gland?

What is the adrenal response to sympathetic stimulation?

A

Receives terminal preganglionic fibres

Stimulation causes release of adrenaline and noradrenaline (30:70)

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5
Q

Which cranial nerves contain preganglionic parasympathetic fibres?

A

CN III, VII, IX, X

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6
Q

What type of fibre are parasympathetic preganglionic neurones?

A

B fibres

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7
Q

What is the distribution of nicotinic AChRs?

A
  • All autonomic ganglia

- NMJ

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8
Q

What is the distribution of muscarinic AChRs?

A
  • Parasympathetic postganglionic synapses

- Sympathetic postganglionic fibres to sweat glands and skeletal vascular smooth muscle

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9
Q

What subtypes of nicotinic receptor have been identified?

A
  • Skeletal muscle
  • Autonomic ganglia
  • CNS pain pathways
  • CNS movement and cognition pathways
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10
Q

Outline the regulation of transmitters at the autonomic ganglion

A

Release of ACh stimulates the postganglionic nicotinic receptor but also activates a muscarinic interneurone which releases dopamine, acting on the presynaptic nerve terminal - providing a feedback mechanism

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11
Q

Contrast the structures and functions of nicotinic and muscarinic AChRs

A

Nicotinic:
-Ligand gated ion channel permeable to Na+, K+ and for some subtypes Ca2+

Muscarinic:
-G-protein coupled receptors classified according to associated second messenger

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12
Q

What is the neurotransmitter at postganglionic sympathetic nerve endings?

A

Noradrenaline

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13
Q

What are the types of adrenergic receptor?

A

α receptors:

  • α1 : postsynaptic
  • α2: usually presynaptic

β receptors:
-β1 + β2 both postsynaptic but also evidence for a presynaptic β2R

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14
Q

What are the excitatory/inhibitory properties of different adrenergic receptors?

A

α: excitatory via increased Na+ permeability

β: usually inhibitory via increased potassium efflux causing hyperpolarisation. Excitatory in the heart.

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15
Q

How does the ANS govern pupillary tone?

A

Symp -> mydriasis (dilatation)

Para -> miosis (constriction)

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16
Q

How does ANS tone affect sweat and salivary gland activity?

A

Symp -> sweating, dry mouth

Para -> no effect on sweating, salivation

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17
Q

How does ANS tone affect hepatobiliary activity?

A

Symp -> Glycogenolysis, gallbladder relaxation

Para -> Glycogenesis, biliary constriction

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18
Q

How does ANS tone affect stomach activity?

A

Symp -> Decreased peristalsis and tone (except sphincters - increased)

Para -> Increased peristalsis and tone, sphincter relaxation

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19
Q

How does ANS tone affect lung activity?

A

Symp -> Bronchodilatation, resultant mild increase in PVR. Equalises flow across lung zones improving V/Q

Para -> Bronchoconstriction, no effect on PVR/flow

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20
Q

How does ANS tone affect cardiac activity?

A

Symp -> Increased HR + contractility, dilated coronary circulation

Para -> Decreased HR + contractility (esp atrial), no effect on coronary flow

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21
Q

Aside from the effects of NA, what other mediators of vascular tone are released by sympathetic terminals?

A

Neuropeptides (eg. Y1)
Purines
ATP

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22
Q

Summarise the baroreceptor reflex

A

^BP -> stretch receptors in carotid sinus and aortic arch -> CN IX + X -> NTS - glutamate release and activation of GABAergic neurones to vasomotor centre -> inhibition of vasomotor stimulation -> vasodilatation

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23
Q

From what levels does the sympathetic outflow occur?

A

T1 - L4

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24
Q

Which systems are involved in co-ordination of movement?

A

Cerebrum - complicated movement
Brainstem and cerebellum - Postural control and balance
Spinal cord - spinal reflexes

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25
Q

What are the components of the spinal reflex system?

A
  1. Sensory neurones:
    - Type Ia/Ib fibres (60-80m/s). Cell body in dorsal root ganglion. Enter cord via dorsal horn.
  2. Motor neurones:
    - Aα fibres (60-80m/s). Exit cord via ventral horn
  3. Interneurones:
    - Most reflex arcs include an interneurone within the grey matter of the cord. These conduct signals between sensory and motor fibres and interact with descending tracts and other interneurones. Enables integrative control.
26
Q

How are skeletal muscle fibres classified?

A

Extrafusal / Intrafusal

Extrafusal:
-Main group, comprising the contractile unit. Innervated by α-motor neurones.

Intrafusal:
-Part of muscle spindle. Innervated by γ-motor neurones (2-30m/s)

27
Q

How are skeletal muscle sensory units classified?

Outline their function

A

Muscle spindles / Golgi tendon organs

Muscle spindles:
-Respond to length/rate of change. Stimulate reflex contraction to reduce stretch

Golgi tendon organs:
-Adjacent to myotendinous junction. Sense stretch. Each organ innervated by single afferent sensory Ib axon

28
Q

What is the structure of a muscle spindle?

A

Up to 10 intrafusal muscle fibres (parallel to extrafusal fibres) enclosed in a connective tissue capsule.

2 types of intrafusal fibre in the spindle:

Nuclear bag fibre:

  • Multiple nuclei in a dilated central part of the spindle
  • Involved in dynamic and static response to stretch

Nuclear chain fibre:

  • Thinner, no bag.
  • Involved only in static response to stretch
29
Q

What is the contractile capacity of the muscle spindle?

How are they innervated?

A

The ends of intrafusal fibres are striated and contractile.

Central portions are non-contractile

Spindles are supplied by γ-motor neurones which regulate the sensitivity of the stretch receptor reflex through contraction/relaxation of the peripheral spindle. Contraction stretches the central portion and increases sensory output.

30
Q

From where do activatory γ-motor neurone impulses originate?

What is the significance of this system?

A

Facilitatory reticular formation

This is the main mechanism for central control of skeletal muscle tone

31
Q

What types of sensory endings are present in the muscle spindle?

A

Primary / Secondary endings

Primary (annulospiral) endings:

  • large fibres encircling central portion of nuclear bag and nuclear chain fibres
  • Type Ia (70-120m/s)
  • Respond to actual length and rate of change

Secondary endings:

  • Smaller Type II fibres encircling ends of nuclear chain fibres
  • Slower conduction speeds
  • Only sensitive to length, not rate of change
32
Q

Outline the tonic control of muscle tension provided by spindle fibres

A

Muscle tone primarily dependent on rate of α-motor neurone discharge

Main influence on the above is rate of discharge of Ia spindle afferents (which are influenced by γ-motor neurone tone)

33
Q

Outline the reflex response to external stretching of a skeletal muscle

A

Increased tone of primary/annulospiral nerve endings dependent on rate of change in length.

Above triggers extrafusal contraction proportional to rate of stretching, which then reduces spindle output.

Following release of stretch -> short period of inhibition of primary nerve endings due to preceding spindle relaxation

34
Q

Describe the structure and function of the Golgi tendon organs

A
  • In series with extrafusal muscle fibres within tendon.
  • Sensory ends lie in between tendon fibres and are squeezed when tendon is stretched - increasing discharge rate.
  • Afferent fibres from Golgi organs synapse with inhibitory interneurones in the cord which synapse with the motor neurone supplying the same muscle.
  • Increased tonic discharge inhibits contraction, preventing damage from overstretching
35
Q

Summarise the stretch reflex

A

Stretch/myotatic reflex:

-Monosynaptic response to stretching of muscle spindle causing muscular contraction

36
Q

Define reciprocal inhibition and explain its role in the stretch reflex

A

Stretch sensory neurones simultaneously synapse with synergistic muscle but also with inhibitory interneurones supplying the antagonistic muscle, causing relaxation. This is reciprocal inhibition

37
Q

Summarise the withdrawal/nociceptive/flexor reflex

A

Polysynaptic

Noxious stimulus -> sensory excitation -> synapse with interneurone -> synapse with motor neurone -> contraction of flexor muscle, withrawing from stimulus

38
Q

Summarise the crossed extensor reflex

A

Polysynaptic. Occurs in conjunction with flexor reflex

Noxious stimulus -> sensory excitation -> synapse with interneurone -> interaction with contralateral interneurones supplying motor neurones of contralateral limb -> contraction of extensors and relaxation of flexors of opposite limb

39
Q

Outline the pathway for conscious movement

A

Initiation in motor cortex -> corticospinal tract -> Spinal interneurones -> integration with cerebellar and spinal reflexes to produce signal to LMN -> movement

40
Q

Outline the hierarchy of perception in postural control

A

Ophthalmic/oculomotor > Vestibular > Neck proprioceptors > Lower body proprioceptors

41
Q

Explain spastic hypertonia following CVA

A

Loss of central modulation of spinal reflexes results in hyperreactivity -> spasticity

42
Q

Describe the nature and course of afferent visceral nerves

A

Unmyelinated fibres travelling from viscera through pre- and paravertebral ganglia (passing rostrally or caudally) on their way to the cord, terminating mainly in superficial dorsal horn

43
Q

What types of sensory afferents innervate the viscera

A

spinal afferents generally signal visceral pain

vagal afferents signal non-painful sensations (eg. hunger)

44
Q

Why is visceral pain poorly localised?

A

Primary visceral afferents are less numerous than somatic afferents.

Several primary visceral afferents may stimulate a single second order spinal afferent.

Thoracic and abdominal viscera also have vagal afferents.

This results in poorly localised (and usually midline) pain.

45
Q

What is visceral afferent convergence?

A

This is the mechanism responsible for referred pain.

Second order neurones receive equal stimulatory input from both somatic and visceral afferents. Stimulation from one can be perceived as the other.

Visceral pain is generally localised to the embryological dermatome of the organ

46
Q

Contrast somatic and visceral pain

A

Somatic: Highly localised, highly differentiated, intensiy proportional to potential tissue damage

Visceral: Poorly localised + differentiated, poor correlation between intensity and potential damage. Association with autonomic Sx

47
Q

What is the phenomenon of pain sensitisation?

A

An increase in magnitude of response to a particular level of stimulation.

48
Q

Why does visceral hypersensitivity occur?

A

Three mechanisms:

  1. Sensitisation of primary afferents
  2. Hyperexcitability of second order neurones (ie. central sensitisation
  3. Dysregulation of descending modulatory neural pathways
49
Q

Discuss central sensitisation syndrome

A

Sensitisation causing allodynia/hyperalgesia

Genetic factors: COMT, 5HTT, ADRB2 polymorphisms

Associated with activation of NMDA receptors in the spinal cord

50
Q

Describe the structure of the NMDA glutamate receptor

A

Ligand-gated Na+/Ca2+ channel

Four subunits (2xN1, 2xN2), each containing four helical domains

N1: each has 1x glutamate binding site

N2: each has 1x glycine binding site

51
Q

What are the different types of visceral pain?

A

True / Referred / Functional

True:
-Vague, diffuse, midline, +-autonomic, allodynia unusual

Referred:

  • Convergence of somatic/visceral neurones
  • Better localised
  • May be associated hyperalgesia

Functional:

  • Pain in absence of structural or biochemical explanation
  • Often features CSS
52
Q

Outline the management options for acute visceral pain

A

Pharmacological / Psychological / Interventional

Pharm:

  • WHO ladder
  • Treat specific cause eg. cardiac pain - nitrates etc. H2 antagonists/PPIs for gastritis. Spasmolytics for IBS

Psych:

  • Physchotherapy
  • CBT
  • Hypnotherapy
  • Good counselling re condition

Interventional:

  • Percutaneous cervical cordotomy (eg. C1/2 lateral spinothalamic tract in mesothelioma)
  • Sympathetic blocks (eg. coeliac plexus, superior hypogastric
53
Q

How may treatment of chronic visceral pain differ from acute visceral pain

A

Evidence for antidepressants in chronic pain.

TCAs / SNRIs / SSRIs

Mechanism not clear but probably involves activation of descending inhibitory pathways. TCAs have multiple possible mechanisms

54
Q

Define neuropathic pain

A

IASP definition:

Pain arising as a direct consequence of a lesion or disease affecting the somatosensory system

55
Q

What are the possible features of neuropathic pain?

A

Positive symptoms:

  • Hyperalgesia
  • Hyperaesthesia
  • Allodynia
  • Dysaesthesia
  • Paraesthesia
  • Hyperpathia

Negative symptoms:

  • Hypoalgesia
  • Hypoaesthesia
  • Hyperpathia

Physical signs:

  • Tropic changes (skin thickening, hair changes)
  • Vasomotor
  • Sudomotor
  • MSK (muscle wasting, osteopaenia)
56
Q

How may neuropathic pain be classified?

A

Central / Peripheral

57
Q

What are possible causes of central neuropathic pain?

A

Spinal cord injury (66%)
MS (30%)
Stroke (30%)

58
Q

What are the possible mechanisms of central neuropathic pain?

A
  • Disinhibition
  • Sensitisation
  • Neuroplastic maladaptive changes to abnormal sensory input
59
Q

What are possible causes for peripheral neuropathic pain?

A

Metabolic: Diabetic neuropathy, Thiamine deficiency
Autoimmune: GBS
Trauma
Ischaemia: CLI
Toxins: chemo, alcohol
Physical compression: TGN, radicular pain

60
Q

What are pharmacological treatments for neuropathic pain?

A
  • Local anaesthetic
  • Capsaicin
  • Baclofen
  • Ketamine
  • Opioids (controversial)
  • TCAs
  • SNRIs
  • Antiepileptics
  • Gabapentin/pregabalin
61
Q

What are some interventional treatments for neuropathic pain?

A

For trigeminal neuralgia:

  • RFA of gasserian ganglion
  • Balloon compression rhizolysis
  • Stereotactic radiosurgery
  • Microvascular decompression (MVD)

Primary FRCA (34 decks)

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