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2nd Year - Systems 3 > Neuro 1 - general structure and function > Flashcards

Neuro 1 - general structure and function Flashcards

1
Q

Cells of nervous system

A

Neurones - dendrites to recieve info - polarised, excitable, terminally differentiated
Microglial cells - immune system to remove debris
Oligodendrocytes (CNS) and Schwann cells (PNS) - produce myelin
Astrocytes - specialized glial cells, form BBB, direct blood flow, transmit info, regulate ion concs
Ependymal cell - line fluid filled cavities, cilia for CSF

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2
Q

Spinal nerves

A

Pair at each vertebral level
Each nerve has separate dorsal and ventral root
Primary afferents have cell bodies in dorsal root ganglion

8 Cervical
12 Thoracic
5 Lumbar
5 Sacral
1 Coccygeal
(31 pairs total)
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3
Q

Plexus vs ganglia

A

PLEXUS
Where 2 or more nerves fuse and then divide to allow redistribution of axons
GANGLIA
Clumps of neuronal cell bodies in specific regions

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4
Q

Afferent vs efferent neurones in PNS

A 
SA - AFFERENT
Sensory
Enter spinal cord by dorsal roots
Somatosensory or viscerosensory
Pseudo-unipolar neurones
ME - EFFERENT
Motoneurones
Leave spinal cord by ventral roots
Somatomotor or visceromotor (controlling autonomic NS)
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5
Q

Somatic vs visceral PNS

A

Somatic - innervate skin, skeletal muscle, joints. Sensory or motor.

Visceral - for emotional reactions beyond voluntary control. Sensory or motor (motor inc sympathetic and parasympathetic).

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6
Q

Sympathetic NS

A

Short preganglionic, long post ganglionic fibres
More sustained action
Travel in sympathetic chain, thoracolumbar T1-L3

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7
Q

Parasympathetic NS

A

Long preganglionic, travel with cranial nerves and S2-4 pelvic splanchnic nerves
Short post ganglionic - paravertebral ganglia close to terminal organs - regional excitation
Energy conserving - discrete, short duration actions

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8
Q

Embryonic development of NS

A

Early in embryonic life, week 3
From ectodermal layer:
- neural groove develops in midline
- neural cells proliferate, form neural tube
- tube will become spinal cord, swells and flexes at cephalic end to form brain

> Neuroblasts become mantle layer around neuroepithelial zone, will become grey matter
Outermost layer, marginal layer, has nerve fibres, myelinated and become white matter

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9
Q

Closure of neural tube (and defects)

A

Anterior neuropore at day 25
- if no, should self-abort. Rarely born, anencephaly - no/unformed brain, will die within hours of life.
Posterior neuropore at day 27
- if no, spina bifida. Less severe, babies born.

To avoid neural tube defects, folic acid before and in early stages of pregnancy.

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10
Q

Cauda equina

A

Below L3, where nerves lie in filum terminale.
– allows space between end of spinal cord and spinal column, can do epidural anaesthetic, lumbar puncture

Because past month 3 of development, vertebral column and dura lengthen faster than neural tube, terminal end of spinal cord shifts higher.
Dural sac and subarachnoid space extend to S2.

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11
Q

Development of brain regions

A

Three primary brain vesicles:
Prosencephalon = forebrain (cerebrum, thalamus, hypothalamus)
Mesencephalon = midbrain
Rhombencephalon = hindbrain (pons, cerebellum, medulla)

Ventricular system formed around 5 weeks

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12
Q

DNA replication in developing brain

A

250,000 new cells / min between 5th week-5th month

  • cells move up to pial surface
  • then move down to ventricular surface
  • DNA aligns
  • vertical cleavage (ascend and descend again to proliferate) or horizontal cleavage (migrate to destination, can’t redivide)
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13
Q

Vertical or horizontal cleavage

A

Transcription factors control gene expression
-> migration to north and south poles
VERTICAL
- daughter cells equal, continue proliferation
HORIZONTAL
- daughter cells unequal, have different fates
- if no numb (only north pole), will become neurones. - migrate by attaching to top of scaffold of glial cells, then
- climb up
-> cortical development, layers of neurones climb up glial cells but inside out, as move through a layer they get info to help them mature - then synapses form, many (surplus), which lose in maturation

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14
Q

Early developmental stages prone to disruption

A

Cortex development especially sensitive to abnormal maturation
- sensitive to genetic mutations and environmental factors (alcohol, thyroid hormone, nicotine, lead, X ray)
Birth defects eg cerebral palsy, low IQ, ADHD, autism

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15
Q

Dura mater

A

Thickest, outer layer of meninges
SUPERFICIAL LAYER = endosteal = periosteum
- continuous with periosteum on outside of skull at foramina
- not continuous with dura of spinal cord
DEEP LAYER = meningeal layer = dura mater proper
- continuous with dura of spinal cord

2 layers always fused apart from at sinus eg superior sagittal sinus: falx cerebri and tentorium cerebelli are sheets going into brain

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16
Q

Arachnoid mater

A

Middle layer
Separated from dura by subdural space - film of fluid
Separated from pia by subarachnoid space - CSF, blood vessels and cranial nerves

Bridges over sulci, doesn’t hug brain
In some areas, projects through dura into venous sinuses - arachnoid villi - oneway valves, allows CSF to drain into sinuses and then veins - reabsorbed as greater hydrostatic pressure in sinus
Collections of arachnoid villi -> arachnoid granulations along sinuses

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17
Q

Pia mater

A

Thinnest, innermost layer
Closesly follows brain surface, extends into sulci
Cerebral arteries entering brain have pia mater covering

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18
Q

Clinical relevance of meninges - haemorrhage

A
  • extradural haemorrhage by damage to meningeal arteries or veins (often middle meningeal A under temporal bone)
  • subdural haemmorhage by damage to cerebral veins -> compression of hemisphere and lateral ventricle
  • subarachnoid haemorrhage by leakage or rupture of cerebral artery circle
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19
Q

Clinical relevance of meninges - headache

A

Brain itself has no pain receptors

So stretching and irritation of the meninges or blood vessels -> headache

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20
Q

Clinical relevance of meninges - meningitis

A

Infection affecting CSF, meningeal irritation

-> inflammation, cerebral oedema, increased ICP, herniation, reduced blood supply

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21
Q

Clinical relevance of meninges - sudden movement of head

A

So brain hits dura/skull

Can damage cranial nerves and blood vessels

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22
Q

Cerebrospinal fluid production

A

150ml total, 25ml in ventricles
Produce 500ml/day
Ultrafiltrate of blood
Active secretion by choroid plexus

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23
Q

Cerebrospinal fluid function

A

Remove waste products
Transport signalling molecules
Renders brain buoyant (reduces effective weight from 1.4kg to 50g)
Supports, cushions, and evenly distributes pressure on brain
Lower concs of K⁺, Ca²⁺, protein, glucose, cholesterol

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24
Q

Choroid plexus

A

= network of capillaries separated from ventricles by choroid epithelial cells
Produce CSF, filters into ventricles
Choroid plexus in lateral ventricles continuous with CP in 3rd ventricle

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25
Q

Blood brain barrier

A

Brain vasculature is basis - endothelial cells with tight junctions
-> brain not usually accessible to rest of body
Move across by:
- paracellular aqueous
- transcellular lipophilic
- transport proteins
- receptor-mediated transcytosis
- adsorptive transcytosis
— may be possible to temporarily open tight junctions to make leaky to drugs, help treatment

Areas around 3rd and 4th ventricles lack BBB to feel fluid/electrocyte balance, hormones etc

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26
Q

Hydrocephalus

A

Blockage in circulation, drainage, or excess production cause increase in ICP
- most likely at narrow passages, interventricular foramen and cerebral aqueduct

In newborn, causes ventricular and skull dilation
In adult, cranial cavity is closed, so headache, vomiting and nausea, increased bp, loss of consciousness, brain stem dysfunction

Treat with shunt to remove excess fluid, or if tumour, remove

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27
Q

Brainstem

A

= medulla oblongata, pons, midbrain
Sensory and motor inputs via cranial nerves to and from head, neck and face
- pineal body - region of diurnal rhythms, synthesise melatonin (only one)

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28
Q

Medulla

A

(part of brainstem)

  • cardiovascular and respiratory control
  • nuclei relay information about taste, hearing, balance, control of neck and facial muscles
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29
Q

Pons

A

(part of brainstem)
- respiration, sleep, taste, bladder control, hearing, swallowing, taste, eye and facial movements, posture, facial sensation

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30
Q

Midbrain

A

(part of brainstem)

  • components of auditory and visual systems - auditory and visual reflexes
  • substantia nigra - part of basal ganglia with key role in Parkinson’s disease
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31
Q

Cerebellum

A

Involved in maintaining posture

  • coordinating head and eye movements
  • fine-tuning movements
  • motor learning
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32
Q

Thalamus

A

(part of diencephalon)

  • for transfer of all sensory info except olfaction - nuclei receive sensory info and then relay to cortex
  • gates and modulates sensory info
  • integration of motor control
  • influences attention and consciousness
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33
Q

Hypothalamus

A

(part of diencephalon)
- regulates homeostasis and behaviours necessary for sexual reproduction - growth, drinking, eating, maternal behaviour, circadian rhythm

Extensive connections to rest of CNS
Connected to pituitary gland for hormonal secretions

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34
Q

Cerebrum

A

Cerebral cortex - ‘higher functions’, perception, motor planning, cognition, emotion, memory - cell arrangement areas according to function

Amygdala - social behaviour and emotion
Hippocampus - memory and learning
(in temporal lobe)

Basal ganglia - control of movements - inc putamen, globus pallidus, substantia nigra, subthalamus, caudate nucleus

White matter - carrying info to and from cortex, between structures

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35
Q

Intracranial pressure

A

CSF makes up 10% of skull contents, but is restricted by dura mater and skull -> increased pressure will eventually compromise respiratory and cardiac centres of brain

Cerebral perfusion pressure = mean BP - ICP
(adult ICP less than 20mmHg, 5-13 normal)
BP needs to be high enough, lower than 70mmHg -> hypoperfusion

Low cerebral perfusion pressure - eg after cardiac arrest
- ischaemic injury occurs at watershed zones - areas between anterior and middle cerebral arteries often

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36
Q

Causes of raised ICP

A

Oedema
Bleeding
Space occupying lesion
Increased CSF / hydrocephalus

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37
Q

Symptoms of raised ICP

A

EARLY
- headache (early morning often) - distortion of meninges and blood vessels
- papilloedema - compression of optic nerve
- vomiting - distortion of medulla
LATE (terminal if left)
- pupillary changes (blown pupil) - compression of occulomotor nerve
- occipital infarction - compression of posterior cerebral artery
- hemiparesis/plegia - compression of cerebral peduncle
- raised bp, decreased HR, pulmonary oedema - compression of medulla
- brainstem haemorrhage - alteration to brainstem arteries

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38
Q

Intracranial herniation

A

1- Cingulate gyrus/subfalcine
2 - Hippocampal uncal/transtentorial -> occulomotor nerve compression, dilated pupil. -> posterior cerebral artery compression, infarction
3 - Cerebellar tonsillar (coning)/foramen magnum -> brainstem compression, damage to vital resp and cardiac centres, fatal
Often due to hypertension

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39
Q

Causes of raised ICP - bleeding

A

Extradural - young, trauma
Subdural - elderly, low force (brain shrinks in so is unsupported, low force hurts)
Subarachnoid - eg berry aneurysm
Intracranial - hypertension

(all can occur in trauma)

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40
Q

Causes of raised ICP - space occupying lesions

A
  • Secondary CNS tumours/mets - SLKBG
  • Primary tumours - rare, as not dividing cells, protected as no direct contact with environment - more in children
  • Gliomas = glial tumours
  • > midline shift, subfalcine herniation, asymmetric lateral ventricals, no edge to tumour (complete resection rare)
  • Meningiomas - better survival

OR

  • Bacterial meningitis
  • Abscesses
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41
Q

Causes of raised ICP - Oedema

A

Cerebral oedema often after infarct/bleed/stroke

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42
Q

Causes of raised ICP - More CSF/Hydrocephalus

A
  • Obstruction = non-communicating, blockage
  • Communicating - no distinct point of obstruction
  • may be due to thickening of arachnoid villi caused by previous meningitis

(‘hydrocephalus ex vacuo’ is not true hydrocephalus, loss of brain tissue in neurodegenerative disease)

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43
Q

Resting membrane potential

A 
Neurones have negative inside membrane potential at rest
Determined by:
- ionic concentration gradients
- ionic electrical gradients
- selective membrane ionic permeability
Intracellular - high K⁺ and organic ions
Extracellular - high Na⁺ and Cl⁻

Electrochemical gradient established by sodium-potassium ATPase - lots of energy used, all neurones constantly using

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44
Q

Nernst equation

A

The equilibrium/nernst potential for ion across a membrane, no net ion movement

Eₓ = RT/zF x ln([extracellular] / [intracellular]

  • only for if ions can move freely, need to take permeability into account (controlled by selective protein ion channels)
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45
Q

Calculating the resting membrane potential

A

Factors influencing movement:

  • concentration gradient
  • voltage gradient
  • membrane permeability

If factor all these in, use Goldman equation:
Eᵣₑ = RT/F x ln (Pk[K⁺ extracellular] + Pk[Na⁺ extracellular] + Pk[Cl⁻ intracellular] / (Pk[K⁺ intracellular] + Pk[Na⁺ intracellular] + Pk[Cl⁻ extracellular]

(inside over outside for -ve ions)
Tells you about all ions and their permeability and effects on cell membrane potential

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46
Q

Ionic basis of action potentials

A 
Synaptic input, EPSP ->
1 - Na⁺ channels open, enter cell
2- K⁺ channels open, leave cell
3 - Na⁺ channels close, K⁺ keeps leaving - at most depolarized
4 - K⁺ close - at most hyperpolarized
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47
Q

Pathological excitability changes

A

Hypokalaemia - hyperpolarized, further from AP threshold
Hyperkalaemia - depolarized, closer to AP threshold, hyperexcitable
(eg strenuous exercise)
Hyponatraemia - less Na⁺ out, (eg SIADH)

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48
Q

Cable properties of the axon

A
  • membrane resistance
  • extracellular and intracellular resistance
  • membrane capacitance
    + myelination sometimes

-> fast, energy efficient, unidirectional propagation

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49
Q

Excitatory synapses

A

Usually cation channels - Na⁺ entry -> postsynaptic depolarisation
(so move towards AP threshold)
GLUTAMATE mainly

Usually anatomically distinct pre and post synaptic elements (boutons and spines)

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50
Q

Inhibitory synapses

A

Usually chloride channels - Cl⁻ entry -> hyperpolarisation
(so move away from AP threshold)
GABA and GLYCINE mainly

Inhibitory and excitatory work together, make oscillations via feedback inhibition -> synchronised, larger effects

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51
Q

Modulatory synapses

A

CATECHOLAMINES - dopamine, NA, adrenaline

MONOAMINES - ACh, 5-HT, histamine

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52
Q

Ionotropic vs metabotropic receptors

A

IONOTROPIC
Ligand-gated ion channels
- eg NMDA type glutamate receptors
Slow

METABOTROPIC
7-transmembrane domain G-protein coupled receptors
- eg group 1 metabotropic glutamate receptors
Fast

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53
Q

Features of neurones + synapses

A

SUMMATION
Critical - at most synapses a single EPSP is not sufficient to drive post-synaptic cell above AP threshold
RATE CODING
As APs are all or none, they cannot carry much info, need firing rates to carry code

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54
Q

Lateral inhibition

A

To sharpen sensory discrimination

  • primary neurone response is proportional to signal strength
  • pathway closest to stimulus inhibits competing neighbours
  • inhibition of lateral neurones enhances perception of stimulus
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55
Q

EEG

A

ElectroEncephaloGram

  • simple, non invasive
  • electrodes taped to head in specific positions
  • voltage changes between pair of electrodes measured
  • select different pairs to examine different areas of brain

Mostly measures excitation of dendrites of pyramidal neurones (80% brain mass)

56
Q

EEG rhythms

A

Types of rhythm correspond to brain activity

DELTA
- slow oscillations in thalamus
- during slow wave sleep
THETA
- quite slow, in medial temporal lobe episodic memory related areas
ALPHA
- restfulness
BETA
- active concentration
GAMMA
- fast, in sensory and memory areas
SHORT BURTS
- fastest, 0.5s spindles (eg twitch in sleep)
57
Q

Somatosensory nervous system

A 
All sensory neural info, except special senses
EXTEROCEPTION - outside world
PROPRIOCEPTION - posture and movement
INTEROCEPTION - internal environment
- info to thalamus then cortex
  • essential for self-preservation and maintenance of body homeostasis
58
Q

Sensory modalities

A

Thermal, mechanical, chemical stimuli
Sensed continually by specific receptors, not necessarily aware unless concentrate

Labelled line concept - separate paths for transmission of info relating to each modality. Integrated at level of cortex.

59
Q

Transduction

A

Conversion of one energy (eg heat, kinetic) to another (always electrical impulses)
Sensory nerve endings have specialised receptors to detect various stimulus modalities - receptor potential
If depolarisation large enough, AP
Intensity of stimulus is rate of AP firing, and more neurones recruited in strong stimuli

60
Q

Modality of afferent sensory neurone

A

Mechanical - mechanoreceptors
Chemical - chemoreceptor
Thermal - cool and warm thermoreceptors
Multiple - polymodal, mixture

61
Q

Threshold of afferent sensory neurone

A

LOW THRESHOLD UNITS
Fire APs from low intensity, innocuous stimuli
Mechano - touch, stroke
Thermo - warm, cool
Chemo - taste, smell (special senses, not afferent sensory)
HIGH THRESHOLD UNITS
Only respond to potentially damaging, noxious stimuli - nociceptors
Mechano - pinch
Thermo - hot, cold
Chemo - acid, adenosine, ATP
—Painful only when reach higher centres of brain

62
Q

Adaptation of afferent sensory neurone

A

When a maintained stimulus of constant strength applied to sensory receptive terminal
-> firing frequency decreases with time
Can be RA (rapidly adapting) or SA (slowly adapting)

  • useful, eg bug, clothes on skin
  • only sees changes in movement (bug moving to sting)
63
Q

Type I sensory receptor fibres

A 
Αα
Wide axon diameter
Myelinated
Fast conduction velocity
Ia - primary receptors of muscle spindle
Ib - golgi tendon organ

Innervate proprioceptors

64
Q

Type II sensory receptor fibres

A 
Aβ
Less wide axon diameter
Myelinated
Fastish conduction velocity
Sensory receptors of muscle spindle, all cutaneous mechanoreception

Innervate proprioceptors and mechanoreceptors

65
Q

Type III sensory receptor fibres

A 
Aδ
Narrow axon diameter
Myelinated (slightly)
Slow conduction velocity
Free nerve endings of touch and pressure, nociceptors of neospinothalamic tract, cold thermoreceptors
66
Q

Type IV sensory receptor fibres

A 
C
Narrow axon diameter
Not myelinated
Slow conduction velocity
Nociceptors of paleospinothalamic tract, warmth receptors
67
Q

Non-nociceptive cutaneous sensory organs

A 
Meissner corpuscle
Pacinian corpuscle
Ruffini's corpuscle
Merkel's discs
Free nerve endings
68
Q

Pacinian (lamellar) corpuscle

A

Non-hairy and hairy skin
1mm long
~40 concentric lamellae - thin, flat Schwann cells - made of fibrous connective tissue and fibroblasts
Wrapped in connective tissue sheath
Fluid-filled cavity with single afferent un-myelinated nerve ending
Detect gross pressure change (poke) and vibration
Large receptive field
Rapidly adapting, low threshold mechanosensitive Aβ fibres

69
Q

Meissner’s (tactile) corpuscle

A

Only non-hairy (glaborous) skin
~50μm long and wide
Mechanoreceptor for light touch and low frequency vibration
Just below epidermis
Rapidly adapting low threshol mechanoreceptor, Aβ fibres
Un-myelinated nerve end enclosed in capsule
Made of elastin attached to epidermis

70
Q

Merkel cells

A

Oval receptor cells found in skin and oral/rectal mucosa and mammary glands
May ‘synaptic contact’ with terminal of slowly adapting low threshold mechanosensitive Aβ fibres
In stratum basale of epidermis, clustered in touch domes
For light touch, discrimination of shapes and textures

71
Q

Ruffini ending

A

Slowly adapting mechanoreceptors in deep sites in skin and joint capsules/ligaments
Spindle shaped end organ made of collagen fibrils
1mm long
Innervated by single Aβ fibre, which branch within corpuscle ending
Monitors tissue stretch

72
Q

Bare ended non-nociceptive fibres

A

Cutaneous thermoreceptors - different units respond across a range of different temperatures
Low threshold mechanosensitive C-fibres

73
Q

Receptors in hairy skin

A

G-hair innervation

  • fulfils roles played by Meissner’s corpuscles in glaborous skin
  • activated by hair movement, esp rapid movements
  • signal through rapidly adapting Aβ fibres

D-hair innervation

  • on finer down hairs
  • rapidly adapting signal through Aδ fibres
  • sensitive to slow movements
74
Q

Muscle spindle

A

Sensory organ in parallel with muscle fibres
In belly of muscle
Signals passive and dynamic muscle stretch
Ia and II sensory fibres

75
Q

Convergence

A

1st order convergence - multiple primary afferents activate single secondary neurone
2nd order convergence - multiple secondary order neurones activate single tertiary neurone

76
Q

Divergence

A

One sensory neurone activates multiple neurones in dorsal column nucleus

77
Q

Somatosensory cortex organisation

A

Neurones in all 6 layers
All cells in a column related to specific location and sensory receptor type
Excitatory and inhibitory connections -> feature extraction

78
Q

Pain

A 
Subjective, multi-dimensional, no need for actual tissue damage
USEFUL:
Alert to tissue damage
Protect injured area
Immobilise
Seek shelter
Promote catabolism
79
Q

Nociception vs pain

A

Nociception - detection of a stimulus which is potentially tissue damaging - can be pleasurable
- can have pain without nociception
- can have nociception without pain
Pain is ALWAYS unpleasant

80
Q

Nociceptive fibres

A 
FIRST PAIN - ouch, withdraw
- Aδ fibres
- 12-30m/s velocity
- pain and temperature
SECOND PAIN - emotional response, vomit, ache
- C fibres
- 1-2m/s velocity
- pain and temperature
81
Q

Cutaneous nociceptors

A

All have free unmyelinated endings
Aδ fibres -> sharp pricking pain
C fibres -> slow burning pain
-> tickle and itch if activated by inflammatory mediators eg histamine

82
Q

TRPV1, capsaicin receptor

A
  • in membrane of C-fibre terminals
  • forms ion channel activated by capsaicin + pungent substances, noxious heat (above 42C), acid pH
  • non-selective cation channel, depolarises cells when active

Activation by heat or capsaicin is enhanced by inflammatory agents, so a burn hurts at room temp also

TRPV1 antagonists block noxious heat detection in man - useful in eg acid reflux pain. But not always good - need to know if burning self, and also used to set normal thermoregulatory system

83
Q

Central sensitisation

A

Wind-up phenomenon
- in dorsal horn neurones in response to stimulation of C-fibres
Substance P and CGRP antagonists can be pain therapies

84
Q

Changes to pain signalling

A

HYPERALGESIA
- increased pain from noxious stimuli
- due to eg inflammation or nerve injury
- part of normal pain response
ALLODYNIA
- pain/unpleasant sensation evoked by low intensity timuli
- due to abnormal activity in primary afferents, or lowered thresholds in CNS circuits involved in nociceptive signalling
- abnormal pain response - neuropathic pain? or eg sunburn

85
Q

Site of first synapses in nociceptive pathway

A

Lamina I

  • Aδ and C fibre primary afferent input
  • from viscera, muscle and skin
  • projection neurones with specific modalities
  • labelled lines, carrying precise information

Lamina II

  • C fibre input
  • from skin
  • modulatory interneurones

Lamina V

  • A fibres (monosynaptic) and C fibres (polysynaptic)
  • wide dynamic range neurones, from many inputs inc nociceptive
86
Q

Nociceptive primary afferent

A 
High threshold
Small cell bodies
C fibres mainly
Substance P and CGRP are peptide content
Neurogenic inflammation possible
Slowly adapting
Synapse at lamina I, II, V
87
Q

Low threshold mechanoreceptive

A 
Low threshold
Large cell bodies
Aα and Aβ fibres
No substance P, little CGRP peptide content
No neurogenic inflammation
Mainly rapidly adapting
Synapse at lamina III, IV, V, VI
88
Q

Spino-thalamic tract

A

Core ascending pathway for nociception

Decussates at spinal level

89
Q

Cortical areas in pain

A

Primary sensory cortex and association cortex (SI and II)

  • relates to pain location
  • contralateral SI and bilateral SII activated

Insular cortex

  • relates to pain intensity
  • lights up when imagine pain

Anterior cingulate cortex
- registers physical pain, codes for its unpleasantness (also roles in emotional function and decision making)

90
Q

Sub cortical areas in pain

A
  • Hypothalamus
  • Medulla + pons
  • Peri-aqueductal gray (PAG)
  • Perebrachial (PB)
  • Amygdala
91
Q

Descending control of nociception

A

Can inhibit sensation of pain via higher centres:
- Periaqueductal gray
- Nucleus raphe magnus
By triggering opioid peptides, serotonin/noradrenaline, inhibit spinal neurones

92
Q

Sites of analgesic opioid action

A

Presynaptic terminals of primary afferent nociceptors
- depresses release of glutamate, so inhibits synaptic excitation

Post-synaptically in spinal cord projection neurones
- inhibit activity of spinothalamic tract by K⁺ channel activation, hyperpolarisation

Periaqueductal gray
- activated PAG projection neurones by inhibiting tonic synaptic inhibition

– CNS can help analgesic, eg hypnosis, and vice versa in stress, sleep loss, sensory isolation etc -> facilitation of pain

93
Q

Projected pain

A

Pain feels like coming from peripheral region, but actual stimulus is somewhere along pain pathway, between nerve to cortex

  • eg sciatica, pain felt in leg, but really nerve irritation at L5/S1 root
    = neuropathic pain
94
Q

De-afferentation pains

A

eg Phantom limb pain (70% of traumatic amputees)

Characteristically:

  • refractory to treatment
  • disabling, associated with anxiety/depression
  • shooting, burning, cramping

Due to - abnormal rewiring centrally, or
- nociceptor activation in stump, body not used to feeling sensation here so projects to old limb

95
Q

Visceral pain

A

Dull, diffuse
Alarming, insidious - receptors may never have been fired, brain confused so may refer to elsewhere (eg in appendicitis)
From stretching of hollow organ, ischaemia, or smooth muscle spasm

Some viscera do not have nociceptors- brain, lung, liver

  • so pain originates in peritoneum, pleura, meninges
  • localisation of source of pain is poor
96
Q

Referred pain

A

Pain perceived at location other than at the site of the painful stimulus
eg angina pectoralis, radiation to left arm, neck, jaw

97
Q

Local anaesthesia definition

A

Local, reversible loss of sensation, without loss of consciousness
- by blocking nerve action potential conduction:
> block Na⁺ channel opening, enhance Na⁺ channel inactivation
> small diameter nerve fibres (eg nociceptive) blocked more readily than large fibres
> in higher concs, other nerve fibres and excitable cells (eg cardiac) blocked

98
Q

Local anaesthetic target fibres

A

Smallest diameter:
Aδ - sharp, pricking pain, temperature
C - slow, burning pain, temperature, itch

(also B fibres in between, sensitive to LAs, but deep inside body so not near target regions for LA)

99
Q

Chemical structure of LAs

A

Aromatic group - lipophilic, hydrophobic, to get into cells

Ester or amide - intermediate chain, link

Amino group - can be protonated, to block Na⁺ channels (can be secondary or tertiary amino groups)

100
Q

Charged and uncharged LAs

A

Uncharged:

  • needed for penetration of neural sheath (rate of onset of action)
  • crossing plasma membrane (access site of action)

Charged:
- needed for interacting with Na⁺ channel

101
Q

Percentage of La ionised/unionised

A

Determined by pH, and pKa of LA (most weak bases, pKa 8-9)
Therefore, at physiological pH 7.4, more ionised than unionised
- in inflammation, pH more acidic, so higher conc ionised molecules, struggles to get into cell, less effective

102
Q

Henderson-Hasselbach equation for a weak base

A

pKa - pH = log ([LAH⁺]/[LA])

% ionised = 100/(1 + 10^(pH-pKa))

103
Q

LA access to site of action

A

Hydrophobic pathway:
- LA diffuse into plasma membrane, then straight into sodium channel to inactivate

MAINLY Hydrophilic pathway:
- unionised LA diffuses across plasma membrane, then becomes ionised, blocks Na⁺ channel

104
Q

Atypical local anaesthetics

A

Benzocaine

  • no amine group, so 0% ionised
  • works via hydrophobic pathway only, less effective

QX-314

  • permanently charged, 100% ionised
  • needs to be introduced straight into cells to block Na⁺ channels (not used clinically)
105
Q

Use-dependence in LAs

A

The more often a neurone fires an AP, greater degree of block
- important in eg antidysrhythmic and antiepileptic drugs, to block rapid AP firing, not normal firing

106
Q

Metabolism of LAs

A

Ester-linked - hydrolysed by plasma esterases, short half life
Amide-linked - metabolised in liver

  • need movement of drug from tissue to blood for anaesthesia to wear off
107
Q

LAs and vasodilation

A
  • some LAs have intrinsic vasodilator properties -> more rapid vascular uptake, shorter duration of activity (removed from site of action, bad)

Vasoconstrictors can be given to prolong anaesthesia, usually adrenaline

108
Q

Clinically used LAs

A

LIDOCAINE - has amide group - most used, rapid onset, moderate duration of action, very stable so long shelf life
BUPIVACAINE - slow onset, long duration, so used for eg spinal block
PRILOCAINE - medium onset, medium duration
TETRACAINE - slow onset, medium duration
ARTICAINE - rapid onset, short duration

109
Q

Clinical uses of LAs

A

Surface anaesthesia - eg throat spray
Infiltration anaesthesia - minor surgeries
Intravenous regional anaesthesia - limb surgery
Intravenous administration - neuropathic pain
Nerve block anaesthesia - MOST
Spinal anaesthesia - for abdomen, pelvis, leg surgery if can’t give GA
Epidural anaesthesia

110
Q

Spinal vs Epidural anaesthesia

A

Spinal

  • subarachnoid space
  • below L2
  • fast onset
  • single dose, so shorter duration

Epidural

  • epidural space
  • cervical, thoracic or lumbar
  • onset slower
  • can place indwelling catheter to maintain dose
111
Q

Adverse effects to local anaesthetics

A

HIGH PLASMA CONC (accidental injection to artery or vein)

  • CNS stimulation, confusion, convulsions, resp depression
  • CVS decrease heart contractility, decrease bp, vasodilation

HYPERSENSITIVITY
- allergic skin reactions

TOXIC METABOLITE
- eg prilocaine, so not used in obstetrics, neonates very susceptible

112
Q

Types of opioid receptors

A

Antagonised by naloxone:
MOP - μ opioid receptor - MAINLY (eg morphine here)
KOP - κ opioid receptor
DOP - δ opioid receptor

Not antagonised by naloxone:
NOP - nociceptin receptor

113
Q

MOP - μ opioid receptor

A

G-protein coupled receptor, 7 transmembrane domains

Activation

  • > closure of voltage sensitive calcium channels
  • > increased potassium efflux, hyperpolarisation
  • > inhibition of adenylate cyclase, decrease cAMP

Full agonist - morphone
Partial agonist - buprenorphine
Antagonist - naloxone

(partial agonist is less potent, useful. But if given with full agonist, will antagonise effects - check not heroin user before give!)

114
Q

Actions of morphine

A

CNS
- analgesia, euphoria, sedation, cough suppression, nausea and vomiting, miosis (pinpoint pupils)

CVS
- depression of vasomotor centre at high doses, mast cell degranulation -> vasodilation, hypotension

RESP
- resp depression, alveolar hypoventilation

GI
- reduced motility, reduced secretions, constipation (so co-prescribe laxative)

GU
- urinary retention

115
Q

Problems with long term use of morphine

A

Tolerance - decreased responsiveness

Dependence - sudden withdrawal -> cold turkey

116
Q

Elimination of morphine

A

Conjugated with glucoronic acid to product secreted in urine (uses liver and kidney)
- adjust to lower dose if patient has hepatic or renal impairment or will overdose

117
Q

Codeine

A

Prodrug, metabolised to morphine

1/10 lack CY2D6 activity, less analgesic effect

118
Q

Fentanyl

A

Synthetic
100x more potent than morphine
Short duration, rapid onset
For intra and post op pain

mcg dose not mg!!

119
Q

Methadone

A

Maintenance therapy for opioid addiction

Blocks euphoric effect if IV heroin is used

120
Q

Naloxone

A

Antidote to opiate overdose
Reverses effects within 2 mins
Lasts 20 mins, need to give shot then put on drip to maintain perfusion until morphine wears off

121
Q

Acute vs chronic pain

A

ACUTE

  • meaningful
  • reversible
  • well defined
  • recent onset
  • clear cause
  • observable signs of tachycardia and hypertension

CHRONIC

  • no longer meaningful
  • irreversible
  • persists over time
  • autonomic adaptation, so may look normal
  • psychological sequelae
122
Q

Neuropathic vs nociceptive pain

A

Neuropathic
- due to injury to peripheral / central nervous system
NERVE PAIN

Nociceptive
- due to stimulation of nociceptors, somatic or visceral

123
Q

Somatic vs visceral pain

A 
(nociceptive)
SOMATIC
- well localised
- aching, throbbing, gnawing
- nociceptors activated in cutaneous and deep tissues

VISCERAL

  • poorly localised
  • deep ache, cramp, pressure
  • may be referred
  • nociceptors activated by stretch or pressure
124
Q

Assessment of pain

A

Severity - 0-10 usually, mild/moderate/severe if can’t manage, faces, visual analogue (plain line)
- ask for now, at best, at worst, average. If say over the scale thats ok!

Never do tests or examinations that wouldn’t alter management.

125
Q

WHO analgesic ladder

A

1 - non-opioids - aspirin, paracetamol
2 - + weak opioid - paracetamol + codeine
3 - strong opioids - morphine, diamorphine

126
Q

Barriers to adequate pain control

A

Opioid adverse effects - constipation, nausea and vomiting, sedation
Attitudes and beliefs - morphine only for really serious pain? stoicism.
Knowledge deficits - tolerance/addiction/side effects risk?
Laws and regulations - sometimes hard to get strong pain relief

Patients with cancer pain do NOT become addicted

127
Q

Use of strong opioids in acute vs chronic pain

A 
ACUTE
- complete relief is goal
- sedation not drawback
- short duration of action ok
- standard dose often
- any route, whichever fastest
CHRONIC MALIGNANT
- pain relief and improvement in function is goal
- sedation undesirable
- need long term effects
- dose is titrated to effect - no limit
- oral route where possible
CHRONIC NON-MALIGNANT PAIN
- goal to improve function
- sedation undesirable
- need long term effects
- dose titrated to effect, within limits
- only ever oral route
128
Q

General anaesthesia

A

Reversible loss of consciousness with absence of sensation
Depresses excitable tissues - nerves and muscles
(too much with depress CVS and resp control centres)`

129
Q

Classes of general anaesthetics

A

Inhalation

  • gaseous and volatile liquids
  • isoflurane, sevoflurane, enflurane, desflurane, nitrous oxide

Intravenous
- propofol, thiopental, etomidate, ketamine

130
Q

Inhalation agents, GAs

A

Speed of induction dependent on solubility in blood and inspired conc
Less soluble, faster effect
Minimum alveolar concentration = conc -> surgical anaesthesia in 50% patients

131
Q

Nitrous oxide, GA

A

MAC > 100%, so cannot produce surgical anaesthesia alone, good with 50% oxygen
Low solubility in blood, rapid onset and recovery (ambulances carry)

132
Q

Halogenated ethers, GAs

A

Isoflurane
Desflurane
Sevoflurane
Enflurane

Can -> malignant hyperthermia rarely, hyper catabolism

133
Q

Propofol

A

Intravenous GA
10-20s onset time, needs constant infusion as short duration also
Metabolised in liver, excreted in urine
‘Milk drug’, white emulsion

(used for pronapping, dangerous)

134
Q

Thiopental (barbituate)

A 
Intravenous GA
Rapid onset, rapid recovery
Metabolised by liver
May depress myocardium and respiratory centre
Used in status epilepticus
'Truth serum'
135
Q

Ketamine

A

Intravenous GA
NMDA receptor antagonist
Stimulates resp and CVS centres
For procedural sedation, hallucinations, induction in status asthmaticus
Abuse -> ulcerative cystitis, bladder removal

136
Q

Depolarising neuromuscular blocker

A

Suxamethonium
Bind to nicotinic receptor at NMJ, inactivate sodium channels
Short half life, for emergency intubation

137
Q

Non-depolarising neuromuscular blocker

A

Attracurium, veruconium, pancuronium
Antagonise NMJ nicotinic receptor
20-40 mins effect

2nd Year - Systems 3 (10 decks)

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