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Semester 3 > Case 9 - Yaffas > Flashcards

Case 9 - Yaffas Flashcards

1
Q

what are the two types of lower motor neurones

A

alpha and gamma

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2
Q

what do the alpha LMNs innervate and what are they involved in

A

extrafusal muscle fibres, and so are involved with the strength and power of a muscle

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3
Q

what do the gamma LMNs innervate and that are they involved in

A

innervate intrafusal muscle fibres, and so are involved with muscle tone and muscle tension

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4
Q

where do individual motor neurone axons branch

A

within muscles to synapse on many different fibres that are typically distributed over a relatively wide area within the muscle

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5
Q

what comes together to constitute the smallest unit of force that can be activated to produce movement

A

a single alpha motor neurone and its associated muscle fibres

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6
Q

what do small alpha motor neurones innervate

A

few muscle fibres and form motor units that generate small forces

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7
Q

what do large motor forces innervate

A

larger, more powerful motor units

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8
Q

what are examples of slow twitch muscle fibres

A

type I, red muscle - ‘slow oxidative fibres’

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9
Q

what are slow twitch muscle fibres innervated by

A

small alpha motor neurones and so form part of small motor units

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10
Q

do slow twitch muscle fibres have a rich blood supply

A

yes - rich capillary beds

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11
Q

why do the muscles appear red

A

rich myoglobin

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12
Q

two more features of slow twitch muscle fibres

A

greatly increased number of mitochondria

resistant to fatigue

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13
Q

what are slow twitch muscle fibres especially important for

A

activités that require sustained muscular contraction, such as the maintenance of an upright posture

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14
Q

examples of intermediate muscle fibres

A

type IIA - fast oxidative glycolytic fibres

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15
Q

features of intermediate muscle fibres

A

they are fast fatigue resistant motor inits and of intermediate size so not quite as fast as FF units

they generate more force than a slow motor unit and, are substantially more resistant to fatigue than an FF unit

they can generate ATP by substrate level phosphorylation (glucose > lactic acid)

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16
Q

what are examples of fast twitch muscle fibres

A

type IIB, white muscle - fast glycolic fibres

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17
Q

what are fast twitch muscle fibres innervated y

A

large alpha motor neurones and so form part of gait fatigueable motor units

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18
Q

what are the large fibres important for

A

great strength of contraction

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19
Q

features of fast twitch muscle fibres that allows for rapid release of calcium ions to initiate contraction

A

extensive sarcoplasmic reticulum

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20
Q

what is found in large amounts in fast twitch muscle fibres that allows for rapid release of energy by the glycolic process

A

large amounts of glycolytic enzymes

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21
Q

other features of fast twitch muscle fibres

A

less extensive blood supply
fewer mitochondria
easily fatigued

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22
Q

what are the principle energy storage molecules utilised by type IIb (fast twitch muscle fibres)

A

creatine phosphate and glycogen

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23
Q

motor unit types summary diagram

A
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24
Q

what is a basic rod-like unit of muscle called

A

myofibril

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25
Q

what are myofibrils composed of

A

actin, myosin, and titin and other proteins that hold them together

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26
Q

how are these proteins organised?

A

into thin filaments and thick filaments, which repeat along the length of the myofibril in sections called sacromeres

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27
Q

what are the thin filaments

A

actin

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28
Q

what are the thick filaments

A

myosin

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29
Q

why do the myofibrils have alternate light and dark bands

A

the myosin and actin filaments partially interdigrate

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30
Q

what do the light bands contain

A

only actin filaments and are called I bands

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31
Q

what do the dark bands contain

A

myosin filaments and actin filaments and are called A bands

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32
Q

where are the ends of the actin filaments attached to

A

a Z disc

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33
Q

features of the Z discs

A

from the Z disc, these filaments extend in both directions to interdigitate with the myosin filaments.

the Z disc passes crosswise across the myofibril and also crosswise from myofibril to myofibril, attaching the myofibrils to one another all the way across the muscle fibres. therefore, the entire muscle fibres has light and dark bands, as do the individual myofibrils. these bands give skeletal and cardiac muscle their striated appearance.

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34
Q

what is the portion of the myofibril that lies between two successive Z discs called

A

the sacromere

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35
Q

digram of muscle fibres

A
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36
Q

what is the sarcoplasm

A

the cytoplasm of muscles

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37
Q

what are the spaces between myofibrils filled with

A

this intracellular fluid

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38
Q

what is this fluid composed of

A

significant amounts of myoglobin, an oxygen binding molecule.

potassium, magnesium and phosphate ions

sarcoplasmic reticulum

protez enzymes

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39
Q

what lie parallel to myofibrils

A

mitochondria

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40
Q

feature of one end of a titin molecule

A

one end is elastic and is attached to the Z disc, acting as a spring and changing length as the sacroemere contrast and relaxes

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41
Q

what is the feature of the other part of the titin

A

tethers it to the myosin thick filament

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42
Q

what is the backbone of the actin filament

A

is the double stranded F actin protein molecule

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43
Q

what is each strand composed of

A

G actin molecules

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44
Q

what is attached to each G actin molecule and what is this thing

A

is one molecule of ADP and this is the active site

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45
Q

what is wrapped spirally around the sides of the F actin helix

A

tropomyosin

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46
Q

what happens in the resting state

A

the tropomyosin molecules lie on top of the active sites of the actin so that attraction cannot occur between the actin and myosin filaments to cause contraction

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47
Q

what is attached intermittently along the sides of the tropomyosin molecules

A

troponin

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48
Q

what does troponin I have a strong affinity for

A

actin

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49
Q

what does troponin T have a strong affinity for

A

tropomyosin

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50
Q

what does troponin C have a strong affinity for

A

calcium ions

51
Q

what is believed to initiate the contraction process

A

the strong affinity of the troponin for calcium ions

52
Q

what is a myosin molecule composed of

A

head, neck and tail

53
Q

what does the myosin head bind to

A

the actin filament

54
Q

what does the myosin head function as

A

an ATPase enzyme

55
Q

what does the myosin neck act as

A

a linker and as a lever arm for transfusing force generated by the motor domain.

the myosin neck can also serve as a binding site for myosin light chains, which have regulatory functions

56
Q

what does the myosin tail connect to

A

the myosin head to the body of the myosin molecule

57
Q

what are the protruding tails and heads together called

A

cross bridges

58
Q

neuromuscular junction, sequence of events.

A

Impulse (action potential) arrives at axon terminal.

Ca2+ ions rush in (as action potential activated Ca2+ gates); Ca2+ reacts with synaptic vesicles.

Synaptic vesicles fuse with cell membrane of axon terminal.

“ACh (acetylcholine) released through a process known as exocytosis.

ACh is synthesised in the axon terminal through the use of ATP. “

“ACh binds with motor end plate receptors: depolarization occurs as Na+ rushes into the
muscle cell, causing an end plate potential (EPP).
ACh is destroyed by acetylcholinesterase.”

Impulse travels through T-tubules which excite the sarcoplasmic reticulum (SR).

Ca2+ ions released from the SR.

Ca2+ binds with troponin.

Shift of tropomyosin, which makes the binding sites available for myosin S1 units to bind.

ATPase splits (hyrolysis) ATP = ADP + Pi + Energy

Myosin can now bind to active sites on actin.

Sliding action of actin over myosin called the Power Stroke.

Impulse stops to muscle; calcium ions pumped back into SR by Ca2+ (active transport) pumps.

Tropomyosin returns over the active sites on actin and muscle action ceases.

59
Q

what destroys ACh and what does this do

A

acetylcholinesterase.

this rapid removal of the acetylcholine prevents continued muscle re-excitation after the muscle fibre has recovered from its initial action potential

60
Q

what does each impulse that arrives at the neuromuscular junction cause

A

about three times as much end plate potential as that required to stimulate the muscle fibres

therefore the normal neuromuscular junction is said to have a high safety factor

however, continuous stimulation of the nerve fibre at great rates diminishes the number of acetylcholine vesicles so much that impulses fail to pass into the muscle fibre. this is called fatigue of the neuromuscular junction

61
Q

what is the resting membrane potential in skeletal fibres

A

about -80 to -90 millivolts

62
Q

what is the motor end point

A

a motor nerve fibre forms a complex of branding nerve terminals that invaginate into the surface of the muscle fibre but lie outside the ,muscle fibre plasma membrane

63
Q

what is the motor end plate covered by

A

Schwann cells that insulate it

64
Q

what happens when the T tubule action potentials act on the membranes of the longitudinal sarcoplasmic tubules

A

causes a release of calcium ions into the muscle sarcoplasm from the sarcoplasmic reticulum, resulting in contraction

65
Q

calcium induced calcium release

A

The T tubule action potentials also open voltage-gated calcium channels in the membranes of the T Tubules themselves, which causes calcium ions to diffuse directly into the sarcoplasm.
The diffusion of calcium ions activates calcium release channels, also called ryanodine receptor channels, in the sarcoplasmic reticulum membrane of the longitudinal sarcoplasmic tubules.
This triggers the release of calcium ions from the sarcoplasmic reticulum into the sarcoplasm.
Calcium ions in the sarcoplasm then interact with troponin to initiate cross-bridge formation and contraction.
This is called calcium-induced calcium release.

66
Q

what would happen without the extra calcium from the T tubules

A

the strength of muscle contraction would be reduced considerably

67
Q

what does the strength of contraction of muscle depend on

A

the concentration of calcium ions in the extracellular fluids

68
Q

what happens at the action potential

A

influx of calcium ions to the interior of the muscle fibre is suddenly cut off, and the calcium ions in the sarcoplasm are rapidly pumped back out of the muscle fibres (via the Na+/Ca2+ exchanger) into both the sarcoplasmic reticulum (SERCA Ca2+ pumps) and the T tubule–extracellular fluid space through the plasma membrane (PMCA Ca2+ pumps), stopping contraction or it is stored in the sarcoplasmic reticulum.

69
Q

what are the four steps of muscular contraction

A
  1. ATP is hydrolysed when myosin head is unattached. the hydrolisation of ATP into ADP and inorganic phosphate allows the myosin head to return to the resting position
  2. ADP+ P are bound to myosin as myosin head attaches to actin
  3. ADP+P release causes head to change position and actin filament to move
  4. binding of ATP causes myosin head to return to resting position. binding of ATP causes myosin head to detach from the actin filament.
70
Q

how does the contraction force increase

A

the greater number of cross bridges in contact with the actin filament at any given time

71
Q

what happens in contraction

A

H and I bands shorten
A ands stay the same size

72
Q

what are the two ways that summation occurs in skeletal muscle contraction

A

by increasing the number of motor units contracting simultaneously, which is called multiple fibre summation

bu increasing the frequency of contraction, which is called frequency summation and can lead to tetanisation

73
Q

what are the 4 different types of muscle contraction

A

isometric
isotonic
concentric
eccentric

74
Q

what is isometric muscle contraction

A

when the muscle does not shorten during contraction. the length of the muscle remains unchanged. e.g pushing against a wall

75
Q

what is isotonic muscle contraction

A

when length of the muscle shortens but the tension on the muscle remains constant throughout the contraction

76
Q

what is concentric muscle contraction

A

in the direction of contraction of a muscle

77
Q

what is eccentric muscle contraction

A

in the opposite direction of contraction of a muscle

78
Q

what is creatine phosphokinase

A

phosphocreatine contains high energy phosphate bonds which can be used to phosphorylate ADP to ATP by the enzyme creatine kinase

it is located in the Z line

79
Q

what is myokinase

A

catalyses the transfer of a phosphate group from one ADP molecule to another to form ATP and the by product adenosine monophsophate

this is known as the last gap of short term energy stores

80
Q

what happens in the metabolism with muscle contraction

A

In normal muscular contraction, glucose is covered into pyruvate and then CO2. this requires ATP via oxidative phosphorylation.
there is plentiful ATP but the process is slow

81
Q

metabolism in intense muscular contraction

A

glycogen is converted into glucose and then lactate. this requires ATP via substrate level phosphorylation. there is limited ATP but the process is fast. oxygen and nutrient supply is rate limiting

82
Q

what is the Cori cycle

A

oxygen is used by the liver to produce glucose from lactate

83
Q

what does muscle hypertrophy result from

A

an increase in the number of actin and myosin filaments in each muscle fibre

84
Q

what is fibre aplasia

A

the rate of synthesis of muscle contractile proteins is far greater when hypertrophy is developing in turn, some of the myofibrils themsevles have been observed to split within hypertrophying muscle to form new myofibrils

85
Q

what happens when a muscle remains unused for many weeks

A

the rate of degeneration of the contractile proteins is more rapid than the rate of replacement

therefore, muscle atrophy occurs

the pathway that appears to account for much of the proteind graduation in a muscle undergoing atrophy id the ATP dependent ubiquitin proteasome pathway

86
Q

what does loss of innervation to a muscle result in

A

atrophy

87
Q

what happens after about 2 months

A

proteasome degradation, causing further muscle wastage

88
Q

if the muscle is innervated again, when is full recovery made

A

within 3 months

89
Q

what are the muscle fibres replaced with in the final stage of denervation atrophy

A

fibrous and fatty tissue

90
Q

what does the fibrous tissue have a tendency to continue doing

A

shortening for many months which is called contracture

91
Q

what can exercise lead to an increase in

A

muscle mitochondrial biogenesis

92
Q

how does this happen

A

This is probably via Ca2+ signalling pathways in the cell as well as via a chronic imbalance of ATP demand versus ATP production by mitochondria which causes activation of signalling protein kinases.

93
Q

what is AMPK

A

adenosine monophosphate-activated protein kinase:

This enzyme plays a role in cellular energy homeostasis.
This is the ‘fuel gauge of the cell’.
During a bout of exercise, AMPK activity increases while the muscle cell experiences metabolicstressbrought about by an extreme cellular demand for ATP.
Upon activation, AMPK increases cellular energy levels by inhibitinganabolic energy consuming pathways (fatty acidsynthesis,protein synthesis, etc.) and stimulating energy producing,catabolic pathways (fatty acid oxidation, glucose transport, etc.).

94
Q

what does lack of exercise lead too

A

atrophy in muscles

Skeletal muscle atrophy causes a drop in:
Protein levels, fibre diameter, force production, and fatigue resistance.
A reduction in protein synthesis coupled with increased protein degradation pathways contribute to muscle loss due to disuse.
Proteolytic pathways (ubiquitin-proteasome, lysosomal, and calpain) are involved in muscle atrophy.
Transcription factor NF-κB and myostatin are important cell signallers for muscle cell atrophy. Lack of exercise leads to increase in these factors in muscle.

95
Q

what does the gait cycle consist of

A

one cycle of swing and stance by one limb

96
Q

what does the stance phase begin with

A

heel strike, when the heel strikes the ground and begins to assume the bodys full weight and ends with a push off by the forefoot - a result of plantarflexion

97
Q

what are the four phases of the stance phase and what are the muscles used in each

A

Heel strike (initial contact) – Gluteus maximus and Tibialis anterior

Loading response (foot flat) – Quadriceps femoris

Midstance – Soleus and gastrocnemius (together known as Triceps surae)

Terminal stance (heel off) – Soleus and gastrocnemius (Triceps surae)

98
Q

when does the swing phase start

A

begins after push off when the toes leave the ground and ends when the heel strikes the ground

99
Q

what are the 3 phases of the swing phase and what are the muscles used

A

Preswing (toe off) – Rectus femoris

Initial and Midswing – Iliopsoas and rectus femoris

Terminal swing – Hamstrings, Tibialis anterior and Ankle dorsiflexers

100
Q

how much of the walking cycle does each phase take up

A

the swing phase takes up 40% and the stance phase takes up 60%

101
Q

why is the stance phase longer

A

because it features a period of double support as the weight is being transferred from one leg to the other

in running, there is no period of double support

102
Q

what are local circuits in the spinal cord called

A

central pattern generators

103
Q

what are these central pattern generators fully capable of controlling

A

the timing and coordination of complex patterns of movement, and of adjusting them in response to altered circumstances

104
Q

what is the Romberg’s test

A

With the eyes open, three sensory systems provide input into the cerebellum to maintain truncal stability.
These are vision, proprioception, and vestibular sense.
Ask the subject to stand with their feet together without support, first with their eyes open and then with their eyes closed.
Closing the eyes eliminates vision.
If the proprioception and vestibular pathways are intact the subject will not sway.
If patient sways - Romberg positive.
If the subject sways with their eyes closed this indicted a defect in their proprioception pathways.
If the patient starts to sway with their eyes open or closed, this indicates a cerebellar lesion.

105
Q

what is a stress fracture

A

a fracture occurring in normal bone that has been subject to excessive and repeated trauma resulting in cumulative microscopic fractures.

over time these micro-fractures exceed the capacity of normal healing resulting in the development of a macro fracture

106
Q

how is stress fracture diagnosed

A

initially X rays are normal. but a bone scan or MRI will usually allow diagnosis to be made

107
Q

what is the treatment for a stress fracture

A

protected weight bearing, rest, cross training and surgery

108
Q

what is an osteophyte

A

these are bony projections that occur at the sites of cartilage degeneration or destruction near joints and intervertebral discs.
They are usually shaped like a rose-thorn.

109
Q

why do osteophytes form

A

because of the increase in damaged joint’s surface area.
This is most common from the onset of arthritis.
Osteophytes limit joint movement and typically cause pain.

Osteophyte formation is related to sequential and consequential changes in bone formation that is due to aging, degeneration, mechanical instability, and disease.

110
Q

why do more men than women get ACL injuries

A

Physical conditioning
Muscular strength
Neuromuscular control
Pelvis size – females have wider hips and so working their legs will cause the vastus lateralis to develop more than the vastus medialis, thus pulling the patella laterally and causing the tear in the ligament.
Lower extremity (leg) alignment
Increased looseness in ligaments
Effects of oestrogen on ligament properties

111
Q

what are the three bones that meet to form the knee joint

A

the femur, tibia and patella

112
Q

what are the 4 primary ligaments of your knee

A

medial and lateral collateral
cruciate ligament
posterior

113
Q

what type of imaging shows an ACL injury

A

MRI

114
Q

how are ACL tears surgically repaired

A

the ligament must be reconstructed
replaces the torn ligament with a tissue graft th
this graft acts as a scaffolding for a new ligament to grow on
may take up to 6 months recovery

115
Q

what is the female athlete triad syndrome

A

syndrome of 3 interrelated conditions which include
- eating disorder
- menstrual dysfunction
- decreased bone mineral density

116
Q

what is the two types of amenorrhoea

A

Primary amenorrhoea, which is the absence of menstruation by the age of 16.

Secondary amenorrhoea, which is the absence of menstruation for 3 months in a woman who has previously had cycles.

117
Q

can hyperprolactinamyia cause amenhorrhoea

A

yes

118
Q

what is shin splints

A

This is described as pain along the inner edge of the shinbone (tibia).
They are a common injury affecting athletes who engage in running sports or other forms of physical activity.
Most prevalent lower leg injury.
It ischaracterised by general pain in the lower region of the leg between thekneeand ankle.
They are caused by repeated trauma to theconnectivemuscle tissuesurrounding thetibia.

119
Q

what Is pain associated with shin splints caused from

A

disruption of Sharpey’s fibres that connect the medial soleus fascia through the periosteum of the tibia where it inserts into the bone

120
Q

when is the impact worsened

A

by running uphill, downhill on uneven terrain or on hard surfaces

121
Q

what is patient/agent driven decision making

A

physician presents all options and the patient makes his or her own choice physician provides no recommendations

122
Q

what is physician recommendation decision making

A

the physician explains all the options and also makes a recommendation

123
Q

what is shared decision making

A

the patient and the physician work together to reach a mutual decision

124
Q

what is the link between osteophytes and amenhorrhea

A

loss of oestrogen can damage bone health - low bone density

Semester 3 (94 decks)

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