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Medicine phase 2 limbs and back > week 3 - nerve, muscle and movement > Flashcards

week 3 - nerve, muscle and movement Flashcards

1
Q

how to increase the force of a muscle movement

A

more complete activation of one muscle
more activation of agonist muscles
more inactivation of antagonist muscles

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2
Q

muscle fascicle

A

bundle of cells (fibres) surrounded by connective tissue

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3
Q

motor unit

A

single motor neurone and all the muscle fibres it innervates

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4
Q

what is the number of motor units dependent on

A

muscle size and the muscle function

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5
Q

what is the number of muscle fibres in a motor unit dependent on

A

muscle function

small motor units give good force control eg. hands

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6
Q

can a muscle contain motor units with different properties

A

yes some muscles contain slow and fast motor units

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7
Q

describe the connective tissue in a muscle

A

epimysium - dense irregular collagenous connective tissue surrounding the entire muscle
perimysium - surrounds fascicles and is derived from epimysium
endomysium - surrounds muscle cells

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8
Q

types of muscle fibres

A 
red fibres (type I)
white fibres (IIa and IIb)
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9
Q

difference between muscle fibre types

A

red fibres - thin, abundant mitochondria, contract weakly and slowly but for long period
white fibres - larger, fewer mitochondria, brief but powerful contractions

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10
Q

difference between type IIa and type IIb muscle fibres

A

IIb use glycolysis almost exclusively to fuel contractions and fatigues rapidly
IIa uses a combination of oxidative metabolism and glycolysis - fatigues at intermediate rates

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11
Q

types of motor unit

A 
slow (s or type 1)
fast fatigue resistant (FFR, 2a)
fast fatiguing (FF, 2b, 2x)
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12
Q

properties of the different motor units

A

type 2x has a larger force/twitch, not many high force contractions and faster fatigue
type 1 has a smaller twitch, slower rise, slower fatigue

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13
Q

effects of strength training

A

early changes - better motor unit activation, less antagonist activation, improved glycolytic metabolism
after 6 weeks - FF fibre hypertrophy

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14
Q

effects of endurance training

A

enhanced oxidative metabolic profile, more mitochondria, improved O2 supply, more myoglobin, S and FFR fibre hypertrophy

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15
Q

which fibre type is associated with good endurance

A

type I fibres

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16
Q

which fibre type is associated with strength training (high force output)

A

type II fibres

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17
Q

what is fatigue

A

inability to maintain power output, reversible by rest

reduces force and power

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18
Q

causes of peripheral fatigue

A

failure of excitation-contraction coupling, t tubule action potential, SR activation, Ca++ release
failure of force generation at cross bridges
failure of ATP generation by depletion of energy stores

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19
Q

causes of central fatigue

A

loss of excitability of motor cortex - probable reflex inputs from metabo-receptors in muscle
can also include failure of transmission in peripheral nerve and NMJs

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20
Q

what is a nociceptor

A

pain receptor - sensory neuron that responds to damaging or potentially damaging stimuli by sending “possible threat” signals to the spinal cord and the brain

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21
Q

what is a mechanoreceptor

A

receptor that relays extracellular stimulus to intracellular signal transduction through mechanically gated ion channels. The external stimuli are usually in the form of touch, pressure, stretching, sound waves, and motion

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22
Q

what is an ergoreceptor

A

Any of the sensory receptors in muscle that detect chemical by-products of skeletal muscle contraction and relaxation - tells you how hard the muscle is working

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23
Q

main tasks for cardiovascular system during exercise

A

to provide adequate oxygen to fulfil metabolic demand of exercising muscles and to guarantee metabolic end-products washout
to regulate arterial blood pressure in order to maintain adequate perfusion of the vital organs without excessive pressure variations

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24
Q

Describe the excitation failure in t-tubules during fatigue

A

high AP firing rate leads to extracellular accumulation of K+
this makes some t-tubules inexcitable and impair excitation contraction coupling
recovery from this type of fatigue will be rapid as K+ concentrations are restored by ion pumping and diffusion

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25
Q

what happens to muscle if ATP runs out

A

muscle goes into rigor not fatigue

rigor muscles do not move - rigid

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26
Q

changes to ADP, Pi and H+ conc in fatigue

A

all increase - this impairs calcium fluxes and impairs force delivery at cross bridges

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27
Q

impairment of calcium fluxes in fatigue

A

ADP, Pi and H+ all inhibit Ca++ release and uptake into SR
this affects force and speed of shortening and relaxation
H+ also competes with Ca++ for troponin binding

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28
Q

describe lipid recruitment in exercise

A

during long duration exercise, lipid metabolism starts after ~90% or the initial glycogen has been used
lipids come from adipocytes and intramuscular stores
very long duration activities utilise lipids almost entirely

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29
Q

describe the different motor unit use in different types of exercise

A

long duration exercise - low power, uses type 1 (slow fatiguing)
moderate duration exercise - higher power, uses type 1 and type 2 (slow and FFR)
short duration exercise - higher power, all units active

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30
Q

describe metabolism differences in different exercise durations

A

long duration - aerobic, good at carbohydrate and lipid metabolism
moderate duration - aerobic, fuel mix uses more carbohydrate
short duration - includes aerobic and anaerobic metabolism, carbohydrate metabolism, inefficient glycolytic metabolism

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31
Q

changes to fibres in endurance training

A

type 1 fibres may enlarge
reduced number of type 2x
type 2a response varies
(selective hypertrophy of S and FFR fibres)

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32
Q

changes to fibres in strength training

A

type 2x, 2b and 2a fibres enlarge

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33
Q

describe the phases of strength gain

A

neural - first 4-6 weeks - activation of motor units improves
hypertrophic - development of new contractile proteins which are added laterally to existing myofibrils, later there is fibril splitting where the most enlarged fibrils divide longitudinally - large motor units grow
connective tissues also strengthen

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34
Q

improvements due to endurance training

A

improved cardiovascular performance - improves O2 delivery: cardiac output, better regional flow, higher capillary density, blood volume
improved metabolic performance - improved enzyme concentrations, improved mitochondrial density, better substrate storage and mobilisation

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35
Q

structure of a neuron

A

cell body has the nucleus
axon relays info from cell body to axon terminals
axon terminals released NTs to activate target of the nerve cell

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36
Q

direction of sensory neurons

A

afferents - towards CNS

37
Q

direction of motor neurons

A

efferents - to muscle

38
Q

two types of axons in a peripheral nerve

A

myelinated axons and unmyelinated axons

39
Q

describe myelinated axons

A

they have a series of schwann cells lined up along the axon, each having a wrapped coating of myelin insulating the axon

40
Q

describe unmyelinated axons

A

encased by schwann cell cytoplasm but there is no wrapped coating of myelin surrounding the axons

41
Q

differences between myelinated and unmyelinated axons

A

M - larger diameter, faster AP conduction - touch, vibration, motor
UM - pain, thermal (hot and cold)f

42
Q

connective tissue in a peripheral nerve

A

epineurium - connective tissue surrounding the peripheral nerve
perineurium - connective tissue surrounding fasicle

43
Q

describe a pseudounipolar neuron

A

sensory afferents

axon from cell body splits into 2 - one branch to periphery and a branch to the CNS

44
Q

what do mechanoreceptors respond to

A

mechanical deflection, touch

45
Q

what do thermoreceptors respond to

A

hot/cold

46
Q

what do nociceptors respond to

A

noxious (pain)

47
Q

what does the dorsal horn contain

A

cell bodies of sensory neurons

48
Q

what does the ventral horn contain

A

cell bodies of motor neurons

49
Q

organisation of spinal cord segments

A 
C1-8 
T1-12
L1-5
S1-5
C1
50
Q

how many spinal nerves does each spinal segment give rise to

A

each segment gives rise to a pair of spinal nerves

51
Q

cervical plexus

A

C1-5

innervates neck

52
Q

brachial plexus

A

C5-T1

upper limb innervation

53
Q

lumbrosacral plexus

A

T12-S5

lower limb innervation

54
Q

nerves of the brachial plexus

A 
axillary
musculocutaneous
radial
ulnar
median
55
Q

spinal segments and the muscle they innervate

A 
C3, 4, 5 - diaphragm
C5 - deltoid
C5, 6 - biceps brachii, brachialis
C6, 7 - extensor carpi radialis, longus and brevis 
C7, 8 - triceps brachii
C8 - flexor digitorum, superficialis and profundus
C8, T1 - interossi 
L2, 3 - adductor longus and brevis 
L3, 4 - quadriceps 
L4, 5 - tibialis anterior 
L5, S1 - extensor hallucis longus
S1, 2 - gastrocnemius and soleus
S2, 3, 4 - sphincter ani extemus
56
Q

how is the extent and level of a spinal injury evaluated

A

ASIA scale - clinicians consider voluntary movement, reflex movement, sensory responses and awareness of body parts

57
Q

pathway for voluntary movement

A

upper motor neuron to lower motor neuron

upper recruits lower

58
Q

difference in the pathway for reflex movements and voluntary movements

A

no upper motor neuron component in reflex

59
Q

inducing spinal reflexes

A

relax limb - tap on tendon - stretches the muscle

biceps, triceps, ankle and rectus abdominis all have jerk reflexes

60
Q

disruption of the motor pathway in paralysis

A

disruption in lower motor neuron component means muscle wont contract - no reflexes and no voluntary movement
disruption in upper motor neuron means no voluntary movements below the level of the lesion but reflexes persist

61
Q

causes of upper and lower motor neuron damage

A

upper - stroke, lesion of axons eg. SCI

lower - motor neuron disease, lesion of motor axon

62
Q

what is gastrulation

A

process of cell division and migration resulting in the formation of the 3 germ layers

63
Q

regions of the mesoderm layer

A 
notochord
paraxial mesoderm
intermediate mesoderm 
lateral plate mesoderm 
extraembryonic mesoderm
64
Q

role of the paraxial mesoderm

A

forms from cells moving bilaterally and cranially from the primitive streak
lies adjacent to notochord and neural tube
forms the somites in the embryo

65
Q

role of the intermediate mesoderm

A

forms genitourinary system

66
Q

describe the lateral plate mesoderm

A

split by a cavity (intraembryonic coelom) into 2 layers:
somatic or parietal layer
splanchnic or visceral layer

67
Q

notochord function

A

signalling centre - controls specification of surrounding cells
important in sending signals to ectoderm and in development of NS
influences somite formation

68
Q

what are the oropharyngeal and cloacal membranes

A

only regions in the embryo with no mesoderm
oropharyngeal membrane breaks down to form mouth
clocal membrane breaks down to form anal canal

69
Q

origin of each muscle type

A

skeletal - paraxial mesoderm
smooth - visceral layer, lateral plate mesoderm around gut tube
smooth - ectoderm or splanchnic mesoderm
cardiac - visceral layer, lateral plate mesoderm around heart tube

70
Q

somitogenesis

A

paraxial mesoderm gets organised into segments called somites
form alongside the developing neural tube in a craniocaudal sequence over time from day 20
appear at approx 3 pairs a day until the end of week 5
controlled by a number of genes

71
Q

regulation of somitogenesis

A

FGF family, Wnt and notch - tell cells to switch between a permissive and non permissive state in a constantly timed fashion
a wave of factors then sweeps along the embryo and interacts with cells that are permissive (switched on) at the right time in the right area
notch needs to be on for somite formation - then switches off
FGF8 travels in opposite direction and controls somite formation when it gets to cells expressing notch

72
Q

role of somitogenesis

A

42-44 pairs at the end of week 5 - forms axial skeleton

73
Q

what is a somite

A

a block of paraxial mesoderm that gives rise to skeletal muscles

74
Q

describe somite differentiation

A

cells in ventral and medial area undergo an epithelial mesenchymal transition - becomes the sclerotome - forms vertebrae and ribs
cells in dorsal half form the dermomyotome

75
Q

what does the dermomyotome form

A

splits into dermatome (forms the dermis of the back) and the myotome (forms muscles)

76
Q

what do the lateral plate mesoderm layers form

A

parietal - body wall, CT and bones

visceral - wall of gut tube, serous membranes

77
Q

what are myocytes

A

mature muscle cells

made from myoblasts which are muscle cell precursors

78
Q

differentiation of myoblasts

A

myoblasts align into chains and fuse, cell membranes disappear creating multinucleated myotubes
myogenin mediates this differentiation
when growth factors are depleted:
myoblasts stop dividing
myoblasts then secrete fibronectin onto ECM, bind to it via an integrin-crucial step

79
Q

function of MYOD and MYF5 in muscle development

A

transcription factors that activate muscle-specific genes
enable the differentiation of myogenic precursor cells in the dermomyotome into myoblasts
can convert non-muscle cells to cells expressing all the muscle proteins = muscle cell
MYF5 required for myoblast formation

80
Q

how are MYOD AND MYF5 activated

A

WNT proteins and BMP combine to activate MYOD in the dermomoytome - creates a group of muscle cell precursors which express MYF5

81
Q

inducing sclerotome formation

A

sonic hedgehog and nogin induce it

82
Q

function of wnt family

A

signalling molecules

in development they control - body axis patterning, cell fate specification, cell proliferation and migration

83
Q

function of BMPs

A

GF/cytokine family
control tissue “architecture” throughout body
induce formation of bone/cartilage in development and dysregulated BMP signalling leads to many pathological processes including cancer

84
Q

sonic hedgehog function

A

belongs to hedgehog signalling pathway family

acts as a morphogen (molecule that diffuses to form a conc gradient and has different effects depending on its conc.)

85
Q

function of notch

A

family of transmembrane proteins that control cell fate decisions

86
Q

FGFs function

A

family of cell signalling GFs which activate cell surface receptors
often act as mitogens
in development - often stimulate Wnt signalling
play an important role in mesoderm induction and limb development

87
Q

regulation of smooth muscle cell differentiation

A

serum response factor is responsible for smooth muscle differentiation
SRF upregulated by kinase phosphorylation pathways
myocardin/ myocardin related transcription factors enhance SRF activity

88
Q

skeletal muscle formation

A

myoblasts fuse to form long multinucleated fibres - myotubes
under control of a number of gene sets including MYOD, MYF5 and myogenin
tendons are derived from the sclerotome under control of the transcription factor scleraxis

89
Q

cardiac muscle formation

A

originates from splanchnic mesoderm surrounding the developing heart tube
myoblasts adhere to each oter via intercalated discs
myoD not involved in early cardiac muscle development

Medicine phase 2 limbs and back (6 decks)

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