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Week 5 Flashcards

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1
Q

What do neurones supply

A

Skeletal muscles via somatic nervous system
Smooth muscles via autonomic nervous system
Glands via autonomic nervous system

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2
Q

Causes for degeneration of nerves

A

Acquired causes through injury
Genetics of body
Natural processes of ageing

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3
Q

Which neurones have capacity to regenerate and re-innervate effectors

A

Injured peripheral nerves
CNS neurones don’t regenerate as readily

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4
Q

What does the extent of dysfunction and its severity depend on

A

Nature of the insult to neurone (or its environment)

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5
Q

Structural features of neurone likely to be affected by insult

A

Epineurium (superficial)
Perineurium
Endoneurium
Myelin sheath
Axon (deepest)

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6
Q

What attaches adjacent nerve fascicles

A

Interfascicular bands

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7
Q

What is the system of classification of injuries to nerves based on

A

Degree to which insult reaches depth of tissue
The measure of depth of tissue is given by layers of ensheathing connective tissue

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8
Q

Seddons’ classification of nerve injuries

A

Neuropraxia
Axonotmesis
Neurotmesis

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9
Q

What is neuropraxis

A

When a neurone temporarily loses its ability to function normally this is known as neuropraxis
-injury would be most probably at level of myelin sheath only
-restoration of function would be complete, upon recovery

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10
Q

What is axonotmesis

A

Usually result of a severe crush injury to a peripheral nerve
Axons of nerve together with their myelin sheaths are damaged
The endoneurium, perineurium, epineurium remain intact
Motor and sensory nerves are affected in same way
Restoration of function can be expected to return fully

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11
Q

What is neurotmesis

A

When the entire nerve fibre is completely transected or severed
It’s the most severe class of nerve damage according to seddon’s classification system
The axon and connective tissue of nerve are all damaged
Recovery of function doesn’t occur in such nerve injuries

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12
Q

What is the proximal segment

A

Likely to continue to receive support of cell body
Survives injury

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13
Q

What is the distal segment

A

Often cut off from cell body
Loses potential for repairs
Loses potential for nutritional support
Becomes vulnerable to phagocytosis by glia

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14
Q

3 classes of glial cells

A

Myelin forming cells- oligodendrocytes, Schwann cells
Astrocytes- create an environment in which neurones thrive
Microglia- these are immune cells of nervous system

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15
Q

What happens minutes after injury if sustained

A

The neurone will immediately stop conducting action potentials beyond site of injury
The 2 ends of the cut axon will be exposed and they will start leaking intracellular fluid- axonal transport occurs in both directions
The cut ends will soon pull apart, sealing themselves and swelling at same time

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16
Q

An hour or so after injury is sustained

A

Synaptic terminal degenerates- accumulation of neurofilaments, vesicles
Astroglia surround terminal normally - they react by causing terminals to be pulled away from postsynaptic cell

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17
Q

Fate of the distal segment of a severed nerve

A

The segment of the axon distal to site of lesion is never viable
It soon dies as a result of loss of nutritional support from cell body
The axonal segment undergoes Wallerian degeneration
The axon is digested by phagocytes
Tissues that might be preserved are: myelin sheaths, epineurium, perineurium, Endoneurium
These form hollow tubes to guide any new re growth of the end of proximal end

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18
Q

Days to weeks after axotomy

A

The distal segment stump of axon will undergo Wallerian degeneration (I.e. digested by phagocytes)

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19
Q

Fate of the proximal segment of a severed nerve

A

Days after sustained injury the proximal segment undergoes chromatolysis
The cell body soon becomes very active producing lots of proteins for repairing cell
The volume of the cell body increases and it also becomes bloated with newly synthesised products
The nucleus of cell is consequently displaced from its central position to peripheral margins of cell body
Then injured nerve soon seals wounded stump to form neuroma
This segment doesn’t die, in some cases the nerve stump soon regenerates to innervate peripheral structures

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20
Q

Fate of the axonal stump on proximal segment of axon

A

Regenerating axons form many sprouts some of which find Schwann cell tubes
Severing the axon causes degenerative changes in the injured neuron and in the cells that have synaptic connections with injured neuron

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21
Q

Acute phase of denervation muscle that’s not reinnervated

A

The muscle is immediately paralysed
The muscle will become areflexic
The muscles will start to fasciculate
If muscle is not reinnervated the fasciculations will subside
Muscle will become atonic

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22
Q

Chronic phase of denervation muscle that isn’t reinnervated

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A

As the fasciculations subside the muscle will: lose bulk due to denervation (denervation atrophy), lose bulk due to lack of use (disuse atrophy)
The muscle will die
Muscle tissue will be replaced with connective tissue including fat
This is a state of fibrosis

23
Q

What is rhabdomyolysis

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A

Potentially life threatening disorder caused by breakdown of skeletal muscle resulting in release of various intracellular contents into circulation
This then leads to acute renal failure and possible death
Causes include: crush syndrome in areas of frequent earthquakes , vehicular accidents at high speed

24
Q

What is a reflex

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A

Neural reflexes are stereotyped involuntary reactions of CNS to specific sensory input that can trigger any particular reflex
Produce a rapid response
Somatic and autonomic

25
What is the clinical relevance
Testing reflexes Papillary reflex and deep tendon reflexes
26
What are the general function of reflexes
Constantly adjusting level of skeletal muscle contraction Protective - stop injury and damage, e.g. limb withdrawal, coughing Postural control- e.g. walking Homeostasis- autonomic, e.g. blood pressure
27
What is the reflex arc
Sensory receptor- afferent- integration centre- efferent- effector Communicates with other parts of nervous system
28
What are the neural components
sensory receptors Afferents- sensory neurones Integration centre: interneurones and modulation Efferent neurones Effectors
29
what do the afferents do
Pass through integration centre, part of CNS, brain or spinal cord, might directly synapse with efferent neurones or synapse in between in centre with neurone that lives in integration centre
30
What are interneurones
Not called relay neurones Inbetween sensory and motor neurone Found in CNS, spinal cord, brainstem nuclei , enteric NS (found in gut) Take inputs compute them then output
31
Modulation
Inputs and outputs Clinical relevance Can influence reflex arc action through inputs through other parts of CNS through conscious effort
32
Efferent neurones
Innervate effectors Motor neurones Not just in somatic NS also in autonomic
33
Effectors
Not always skeletal muscle, can be cardiac, smooth or glandular tissue if autonomic reflex Produce an appropriate response to stimulus
34
Simple stretch reflexes (myotatic)
Stimulus- stretch skeletal muscle Changes muscle in response to stretch Posture Adjust degree of skeletal muscle contraction Sensory receptors- proprioceptors Two main types: muscle spindles and Golgi tendon organs
35
What are proprioceptors
Found in muscle, joints and tendons Various points in muscular skeleton They detect joint position and degree of stretching a muscle
36
The muscle spindle
Responds to stretch, stretch receptive sensory receptor Live in skeletal muscle Receptor-Sensory neurone- direct synapse with efferent (alpha motor neurone)- innervating skeletal muscle Made up of specialist muscle fibres, sensory axon wraps round, receptors on nerve endings of sensory axon Monosynaptic reflex arc
37
How does muscle spindle work
Increase in stretch increases sensory activity (increased AP), releases excitatory neurotransmitter, stimulates AP in motor neuron increasing motor activity, NMJ releases ACh, increases contraction- preventing damage
38
Knee jerk reflex uses muscle spindles
Stimulus (stretches quadriceps), AP in afferent, sensory neurone splits into branches, one has a direct synapse with motor neurone which causes muscle (quadriceps) to contract, one forms a synapse with interneurone which releases inhibitory neurotransmitter so motor neurone stops firing AP so muscle (hamstring) doesn’t contract
39
Golgi tendon organ
Sensory receptor for skeletal muscle Reverse (inverse) myotatic reflex Sometimes sensory neurones have nerve endings within tendons within collagen fibres of tendons connecting muscles to skeleton Sensory neurone- inhibitory interneurone within spinal cord- efferent neurone- effector So if activate GTO through lots of contraction cause muscle activity to decrease
40
How to Golgi tendon organs work
Increase in contraction of muscle (pulls on tendons)- increases GTO activation as more AP in sensory neurone- releasing excitatory neurotransmitter- excite interneurone to produce AP- release lots inhibitory transmitter- blocking activity in motor neurone Polysynaptic
41
Function of reverse myotatic reflex
Prevents damage due to overwork Fine control of muscle tension
42
Crossed extensor reflex
Sensory receptors activated- sensory neurone branches many interneurones, some excitatory and some inhibitory, cross spinal cord and synapse with efferents For each leg one muscle is inhibited from contracting and one stimulated to contract
43
Function of crossed extensor reflex
Coordinated stereotype response Coordinating a pair of muscles to be contracted or relaxed Transfer of weight Adjusting postural control
44
Do all reflexes use proprioceptors
No Withdrawal reflex- pain, burning etc
45
Why is it important that local anaesthetics are lipid soluble
LA block voltage gated Na+ channels from the inside of neurons, to gain access to the inside of the neuron they must cross the plasma membrane which is made up of phospholipid and therefore need to be lipid soluble Essential for penetration of both the epineurium and neuronal membrane. The greater the lipid solubility of a drug enhances potency but also enables more rapid diffusion through cell membranes, this hastens the onset for anaesthesia in isolated fibres
46
How do local anaesthetics work
Local anaesthetic agents are amphipathic molecules They bind primarily to Na+ channels but also to K+ and Ca2+ channels and GPCRs Unionised molecules cross neuronal membrane, molecules dissociate to reach new equilibrium of unionised and ionised moieties, dependent on intracellular pH and pKa of anaesthetic. Ionised form binds to open voltage gated Na+ channels in a reversible and concentration dependent manner. Bound molecule stabilises inactivated receptor state preventing further neuronal transmission, nerve block is concentration dependent, increased concentrations inhibit all nerve conduction
47
Local anaesthetics
Competitive antagonists at nicotinic acetylcholine receptors Reversibly block nerve conduction when applied to a restricted area of the body to enable a procedure to be carried out without loss of consciousness Experience of pain reflects damage to the body: detected by nociceptors and converts stimulus into AP
48
Chemical nature of local anaesthetics
Aromatic ring- lipid soluble to cross membranes Basic amine group: equilibrium with water, accepting and donating H+ Aromatic ring and amine group attached by either an ester or amide Ionisation state determined by pH In body larger proportions are ionised than not
49
Mechanism of action of local anaesthetics
De-ionised and ionised forms exist outside the cell Unionised form moves across the membrane into neuron New equilibrium inside the axon: the ionised form blocks open voltage-gated Na+ channels, as it blocks open channels, it is a use dependent block because increase pain means increased open channels Tissue pH affects effectiveness of LA. -inflammation/infection causes more acidic conditions -increased acidity further increases amount of ionised to unionised -means LA cant cross membrane ands has weaker affect
50
Sensory information is divided into 4 categories
Modality Intensity Duration Location
51
Forms of sensory receptors
They each take stimulus energy and transform into neural info- transduction. Type of transduction specific to type of energy used by given sensory system Exteroceptors Interoceptors Mechanoreceptors -mechanical energy Photoreceptors- electromagnetic energy Chemoreceptors- chemical Thermoreceptors- temperature Nociceptors- noxious (chemical, thermal, mechanical), somatic sensory, pain.
52
What is receptor potential
Change in electrical state, a passively conducted change in membrane voltage Intensity of receptor potential is related to intensity of stimulus
53
Generator potential
In other systems (mechanical and olfactory) the receptor specialisations are contained on primary sensory neurones So receptor potential is referred to as generator potential since once the membrane crosses a threshold the neuron generates action potentials
54
Routes of administration of local anaesthetics
Topical- applied directly to skin or mucus membranes, liquids, creams, gels, sprays, patches Infiltration- injection into tissue Nerve block- injected into tissue near major nerve Injected into epidural space/ subarachnoid space in spinal cord

NAS (12 decks)

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