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MSK > Physiology > Flashcards

Physiology Flashcards

1
Q

What is a motor unit?

A

a single alpha motor neuron and all the skeletal muscle fibres it innervates

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2
Q

What does the number of muscle fibres per motor unit depend on?

A

the functions served by the muscle- eg. fine or gross movements

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3
Q

What is the difference between the initation of contraction in cardiac and skeletal muscle?

A

in cardiac it is myogenic (pacemaker potentional) whereas in SK it is neurogenic

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4
Q

What are the factors that determine the gradation of contraction in SK muscles compared to cardiac muscle

A

in SK muscle it is by motor unti recruitment and the summation of contractions whereas in cardiac muscle it depends on the extent of the heart filling with blood

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5
Q

What is excitiation contraction coupling?

A

the process whereby the surface action potential results in activation of the contractile mechanism of the muscle fibre

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6
Q

What stimulates the calcium release from the sarcoplasmic reticulum?

A

when the surface AP spreads down the transverse tubules

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7
Q

What are T-tubules?

A

extensions of hte surface membrane that dip into the muscle fibre

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8
Q

What is the predominant structure of SK muslce fibres?

A

myofibrils

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9
Q

What protein gives the lighter appeanace in myofibrisl?

A

actin

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10
Q

What protein causes the darker appearance in the fibres?

A

myocin

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11
Q

What is the functional unit of muscle?

A

sarcomere

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12
Q

What is the defintion of a sarcomere?

A

the length of a myofibril between 2 Z-lines

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13
Q

What are the Z-lines?

A

they connect the thin filmanets of 2 adjoining sarcomeres

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14
Q

What is the A-band?

A

made up of thick filaments along with portionso f thin filaments that overlap in both ends of thick filaments

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15
Q

What is the H-zone?

A

lighter area within the middle of the A-band where thin filaments dont reach

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16
Q

What is the M-line?

A

extends vertically down middle of A-band within the centre of H-zone

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17
Q

What is the I-band?

A

consists of remaining portion of thin filaments that do not project in A-band (light area)

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18
Q

How is muscle tension produced?

A

sliding of actin filaments on myocin filaments, this is an ATP-dependent interaction

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19
Q

Why is ATP required for both contraction and relaxation?

A

ATP is used to take back calcium into the SR as well power and release the cross bridges (binds to actin to prepare for myosin binding, binds to myosin to unbind it from actin)

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20
Q

How does calcium switch on cross bridge formation?

A

calcium binds to troponin which results in the repositioning of troponin-tropomyocin complex to uncover the cross bridge binding site on actin

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21
Q

What does gradation of SK muscle tension depend on?

A

number of muscle fibres contracting within the muscle and tension developed by each contracting muscle fibre

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22
Q

What is motor unit recruitment?

A

stimulation of more motor units to achieve a stronger contraction

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23
Q

How can motor unit recruitment be done in a way to prevent muscle fatigue?

A

asynchronously

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24
Q

What does the tension developed by each contracting muscle fibre depend on?

A

frequency of stimulation and summation of contrations as well as the lenght of muscle fibre at the onset of contraction

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25
Q

Why is it possible to summate twitches in SK muscle?

A

the duration of AP is much shorter tahn the duration of the resulting twitch

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26
Q

What is twitch summation?

A

when a muscle fibre is restimulated before it has completely relaxed and the second twitch is added onto the first twitch (increasing contraction)

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27
Q

What is tetanus?

A

maximal sustained contraction

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28
Q

When does tetanus occur?

A

if a muscle fibre is stimulated so rapidly that it does not ahve an opportunity to relac at al between stimuli

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29
Q

Why can cardiac muscle not be tetanise?

A

the AP takes as almost as long as the muscle contraction adn there is a long refractory period

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30
Q

What is the optimum length of musche?

A

the point of optimal overlap of thick and thing filmanet cross bridge binding sites and when maximal tetanic tension can be achieved

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31
Q

Is the resting length of SK muscle approx. its optimum length?

A

Yes

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32
Q

What are the 2 types of SK muscle contraction?

A

isotonic contraction and isometric contraction

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33
Q

What is the difference between isotonic and isometric contraction?

A

isotonic contraction is when muscle tension remains constant as the muscle length changes whereas in isometric, muscle tension develops at a constant muscle length

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34
Q

What is isotonic contraction used for?

A

body movements adn moving objects

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35
Q

What is isometric contraction used for??

A

supporting objects in fixed positions and for maintaining body posture

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36
Q

What determines how resistant to fatigue a muscle is?

A

the capacity of the fibre to synthesise ATP

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37
Q

What does the acivtiy of myosin ATPase determine in the muscle cell?

A

the speed at whic henergy is made available for cross bridge recycling- speed of contraction

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38
Q

What is the immediate source for ATP in muscle fibres?

A

transfer of high energy phosphates from creatine phosphate to ADP

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39
Q

What are the 3 types of SK muscle fibres?

A

type 1-slow oxidative
type 2a- fast oxidative
type 2x- fast glycolytic

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40
Q

What are type 1 fibres used for?

A

prolonged relatively low work aerobic activities

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41
Q

What are type 2x fibres used for?

A

short-term high intensity activities

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42
Q

What is the smplest monosynaptic spinal reflex?

A

stretch reflex

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43
Q

What is the purpose of the stretch reflex?

A

negative feedback that resists passive change in muscle length to maintain optimal resting length of muscle

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44
Q

What does activation of the stretch reflex result in?

A

contraction of the muscle

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45
Q

What effect does tapping a muscles tendon have?

A

rapidly stretches the muscle resulting in its contraction

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46
Q

What are the sensory receptors for the stretch reflex?

A

muscle spindles

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47
Q

What are muscle spindles?

A

a collection of specialised muscle fibres

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48
Q

What type of fibre are muscle spindles?

A

intrafusal

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49
Q

What is the sensory nerve ending found in muscle spindles called?

A

annulospiral fibres

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50
Q

What is the name of the special efferent nerve supply for muscle spindles?

A

gamma motor neurons

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51
Q

What is the function of the gamma motor neurons?

A

to adjust the level of tension in the muscle spindles to maintain their sensitivity when the muscle shorten during muscle contraction

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52
Q

What are symptoms of muscle disease?

A

muscle weakness/tiredness
delayed relaxation after voluntary contraction (myotonia)
myalgia
muscle stiffness

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53
Q

What type of axons do motor neurones have?

A

myelinated axons

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54
Q

Where are the cell bodies for motor neurones found?

A

spinal cord or brain stem

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55
Q

what type of axon does the motor neuron branch into near to the muscle?

A

unmyelinated

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56
Q

What does the motor neurone end with that forms a chemical synapse with the muslce membrane at the NMJ?

A

terminal bouton

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57
Q

What horn of the spinal cord are alpha motor neurons cell bodies found?

A

ventral horn

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58
Q

What region of the SK fibre does the bouton synpase?

A

endplate region

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59
Q

What is found in the terminal bouton?

A

ots of mitochondria and vesicles storing ACh

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60
Q

How are vesicles stored in the terminal bouton?

A

clustered awaiting release at active zones

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61
Q

Where are nicotinic ACh receptor found at the NMJ?

A

regions of hte junctional folds that face the active ones

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62
Q

How is choline transported into the terminal?

A

by the choline/Na+ symport transporters

63
Q

How is ACh synthesised in the presynaptic cell?

A

choline and acetyl coenzyme A get converted into ACh by choline acetyltransferase

64
Q

What concentrates ACh into vesicles?

A

vesicular ACh transporter

65
Q

What does arrival of the AP at the presynaptic terminal cause?

A

causes depolarization and the opening of voltage-activated Ca2+ channels and allows calcium entry into the terminal

66
Q

What does calcium do to the vesicles?

A

causes vesicles docked at active zones to fuse with the presynpatic membrane (exocytosis)

67
Q

What causes neuromyotonia?

A

antibodies against voltage-activated K+ channels in the motor neurone resulting in hyperpolarisation as K+ contribute to repolarisation

68
Q

What are nicotinic ACh receptors?

A

a pentamer of glycoprotein subunits that surround a central, cation selective pore

69
Q

What is the permeability of Na+ compared to K+ in the nicotinic ACh receptors like?

A

open cahnnel is roughly equally permeable to both

70
Q

Why is there a greater Na+ influx than K+ efflux?

A

driving force for sodium is greater than for potassium at resting membrane potential

71
Q

What does this depolarisation result in?

A

end plate potential

72
Q

What is the electrical response to one quantum (vesicle) of transmitter called?

A

miniature endplate potential

73
Q

How does an e.p.p trigger an AP?

A

has to exceed threshold

74
Q

What is one to one coupling?

A

one AP in the motor nerve triggers one AP in the muscle and its subsequent twitch

75
Q

What causes the rapid termination of neuromuscular transmission?

A

hydrolisis of ACh by acetylcholinesterase (AChE)

76
Q

What are the symptoms of neuromyotonia?

A

cramps, stiffness, slow relaxation (myotonia) and muscle twitches (fasiculations)

77
Q

What is the cause of Lambert Eaton Myasthnic Syndrome?

A

antibodies against volatge activated calcium channels in the motor neurone terminal results in reduced calcium entry in response to depolarisation and reduced vesicular release of ACh

78
Q

What is the drug treatment for neuromyotonia?

A

anti-convulsants which block voltage activated sodium channels- carbamazepine and phenytoin

79
Q

What are the symptoms of Lambert-Eaton syndrome?

A

muscle weakness in the limbs

associated iwth small cell carcinoma of the lung

80
Q

What are the drug treatment options for Lambert-Eaton?

A

anticholinesterases- pyridostigmine

potasssium channel blockers- 3,4-diaminopyridine which both act to increase the con. of ACh in the synaptic cleft

81
Q

What are the symptoms seen in myasthenia gravis?

A

prograssive muscle weakness during activity (LEMS may transiently improve upon exertion); weakenss of eye and eyelid muscles

82
Q

What causes Myasthenia Gravis?

A

antibodies against nicotinic ACh receptor in the endplate

83
Q

What is the drug treatment for myasthenia gravis?

A

anticholinesterases-edrophonium and immunosuppressants

84
Q

What is the action of vecuronium and atracurium?

A

competitive antagonists of the nicotinic ACh receptors on the end plate reducing the amplitude of the e.p.p to below the threshold for muscle fibre AP generation

85
Q

What are vecuronium and atracurium?

A

induce reversible muscle paralysis in surgery

86
Q

What are the 2 types of fibrous joint?

A

syndesmosis (interosseus membrane) and sutures

87
Q

What are the 2 types of cartilginous joint and give an example of each?

A

synchrondosis-joint between epiphysis and diaphysis in growing bone
symphysis- IV disc

88
Q

What unites the bone in a synovial joint?

A

a fibrous capsule as well as other extra-articular structures

89
Q

What is the inner aspect of the fibrous capsule lined with?

A

synovial membrane

90
Q

What cells produce synovial fliud?

A

fibroblasts

91
Q

What is the difference between a simple and complicated synovial joint?

A

simple has one pair of articular surface whereas a compound joint has more than one pair of articular surfaces

92
Q

What extra-articular structures support the joint?

A

ligamnet; tendon; bursa

93
Q

What is joint lubrication provided by?

A

cartilage interstitial fliud

synovium-derived hyaluronic acid (muscin) and synovium-derived lubrcin

94
Q

Why is synovial fliud not a static pool?

A

the synovial fliud is continuously replensihed and absorbed by the synovial membrane

95
Q

What gives synovial fluid its high viscosity?

A

presence of hyaluronic acid (mucin)

96
Q

What is rapid movement associated with in a joint in terms of viscosity and elasticity?

A

decreased viscosity and increased elasticity

97
Q

In what diseases does the synovial WBC count increase?

A

inflammatory and septic arthritis

98
Q

When does the synovial fliud turn red?

A

in traumatic synovial tap (iatrogenic) and in haemorrhagic arthritis

99
Q

What colour does inflammatory synovial fliud look?

A

straw to yellow

100
Q

from the articular surface to the subchondral bone what are the zones of the cartilage?

A

superficial
middle
deep
calcified

101
Q

What do the cartilage zones differ in?

A

organisation of collagen fibres and relative content of cartilage companents

102
Q

What is the ECM made up of ?

A

water; type 2 colagen and proteoglycans

103
Q

Where is most of the water in the cartilages ECM found?

A

near the articular surface

104
Q

What happens to cartilage water content with age>

A

decreases

105
Q

What is the function of water in the ECM

A

maintains the resiliency of the tissue and contributes to the nutrition and lubrication system

106
Q

What is the function of collagen in cartilage?

A

maintain cartilage architecture and provides tensile stiffness and stregth

107
Q

Where is the highest conc. of proteoglycan found in cartilage zones?

A

middle and depp zone

108
Q

What is proteoglycan mainly composed of?

A

glycosaminoglycan- chondroitin sulphate

109
Q

What is proteoglycan responsible for in cartilage?

A

compressive properties associated with load bearing

110
Q

How does articular cartilage receive nutrients?

A

via the synovial fliud

111
Q

What does the chondrocyte produce that breaks down the ECM?

A

metaloproteinase proteolytic enzymes

112
Q

What factors stimulate proteolytic enzymes and inhibit proteoglycan synthesis?

A

TNF-alpha

IL-1

113
Q

What factors stimulate proteoglycan synthesis?

A

tumour growth factor gamma

insulin-like growth factor-1

114
Q

What are 2 markers of cartilage degradation?

A

serum and synovial keratin sulphate

type 2 collagen in synovial fluid

115
Q

What gives rise to osteoarthritis?

A

cartilage and synovial compostiion and function deteriorate with age and repeated wear and tear

116
Q

What causes rheumatoid arthritis?

A

synovial cell proliferation and inflammation

117
Q

What are the effects on a joint in osteoarthritis? (6)

A 
thickened capsule
cyst formation
sclerosis in subchondral bone
fibrillated cartilage 
synovial hypertrophy
osteophyte formation
118
Q

What is the difference between gout and psuedo-gout?

A

in gout there is depostition of needle shaped uric acid crystals whereas in psuedo-gout there is deposition of rhomboid shaped calcium pyrophosphate crystals

119
Q

What are the 3 forms of pain?

A

nociceptive pain; inflammatory pain; pathological pain

120
Q

What are nociceptors?

A

specific peripheral primary sensory afferent neurones normally actiavted preferentially by intense stimuli that are noxious

121
Q

What type of neurone are nociceptors?

A

first order

122
Q

What is the threshold level for nociceptors?

A

high threshold, provoked only by intense stimuli

123
Q

What are features of nociceptive pain?

A

overrides most other ongoing activites of the nervous system and is extremely unpleasant, inscribing memories to avoid future harm

124
Q

What is inflammatory pain caused by?

A

activation of the immune system in injury or infection

125
Q

What does inflammatory pain cause?

A

pain hypersensitivity and allodynia

126
Q

What is allodynia?

A

innocuous stimuli elicit pain

127
Q

What is pain hypersensitivity?

A

heightened sensitivity to noxious stimuli

128
Q

What is the purpose of inflammatory pain?

A

to assist in healing of a damaged body part

129
Q

What is pathological pain?

A

pain with no protective function that results from abnormal nervous system function

130
Q

What are the 2 types of pathological pain?

A

neuropathic

dysfunctional

131
Q

What is the difference between neuropathic pain and dysfunctional pain?

A

in neuropathic pain there is a neural lesion- actual damage in the nervous system whereas in dysfunctional there is no actual damage

132
Q

What causes pathological pain?

A

abnormal central processing

133
Q

What happens in congenital insensitivity to pain?

A

loss of function mutations in a voltage activated sodium channel that is highly expressed in nociceptive neurones preventing the sensation of pain

134
Q

What are the 2 subtypes of nociceptor?

A

Adelta and C-fibres

135
Q

What type of nociceptor are Adelta fibres?

A

mechanical/thermal nociceptors

136
Q

Are A-delta fibres myelinated or unmyelintaed?

A

myelinated

137
Q

Are C-fibres myelinated or unmyelinated?

A

unmyelinated

138
Q

What type of stimuli do C-fibres receive?

A

all noxious stimuli (poymodal)

139
Q

What type of pain do A-delta fibres mediate?

A

first or fast pain

140
Q

What type of pain do C-fibres mediate?

A

second or slow pain

141
Q

What happens to thermal receptor- TRPV1 in inflammation?

A

greatly sensitised and becomes activated even at body temperature

142
Q

How do the stimuli generate an AP in the receptor?

A

stimulus opens ion channels in nerve terminal to elicit a depolarising potenetial, this amplitude is graded and proportional to stimulus intensity- has to reach threshol to relase AP

143
Q

How does the amplitude of the receptor potential affect frequency of APs?

A

as amplitude increases, frequency proportionally increases

144
Q

Is the relationship between amplitude and stimulus strength linear?

A

no- non-linear which indicates there is a maximum rate at which nerve fibres can fire

145
Q

What horn of the spinal cord do the nociceptor axons synpase?

A

dorsal (posterior) horn

146
Q

What are the 2 tracts that carry pain in the CNS?

A

spinothalamic and spinoreticulothalamic tracts

147
Q

Were are the nociceptor cell bodies found?

A

dorsal root ganglion or trigeminal ganglion

148
Q

How do the afferent nociceptor fibres transmit info to CNS?

A

via release of glutamate and peptides

149
Q

What happens efferently at the nociceptor when there is noxious stimuli?

A

release of pro-inflam mdiators from peripheral terminals

150
Q

What does substance P do?

A

vasodilation and extravasation of plasma proteins (which promote formation of bradykinin and prostaglandins); histmaine release; sensitisation of surrounding nociceptors

151
Q

What is neurogenic inflammation?

A

hyperalgesia and allodynia due to nociceptor release of peptides due to local tissue damage or inflam mediators

152
Q

What are the actions that occur during the neurotrnsmission between the primary afferent adn the second order neurone/

A

AP–opening of voltafe gated calcium channels–calcium influx–glutamate release–activation of glutamate receptors–membrane depolraisation –opening of voltage gated sodium channels–AP

153
Q

Where do primary afferent axons terminate in the dorsal horn of the spinal cord?

A

laminae of Rexed

MSK (39 decks)

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