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LR Musculoskeletal > Physiology > Flashcards

Physiology Flashcards

1
Q

Which of the 3 types of muscles are striated?

A

Striated: skeletal and cardiac muscle

Unstriated: smooth muscle

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2
Q

Striation appears as alternating dark and light bands under the microscope. What makes up the light and dark bands?

A

Dark bands - myocin thick filaments

Light bands - actin thin filaments

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3
Q

Which ion links excitation and contraction?

A

Ca2+

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4
Q

Where does the Ca2+ involved in skeletal muscle vs cardiac muscle contraction come from?

A

Skeletal - entirely from the sarcoplasmic reticulum

Cardiac - ECF and sarcoplasmic reticulum

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5
Q

State what controls the strength of contraction in skeletal muscle (2) vs cardiac muscle (1)

A

Skeletal - motor unit recruitment and summation of contractions

Cardiac - preload

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6
Q

Skeletal muscles are arranged into…

A

Motor units

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7
Q

What are motor units?

A

A number of muscle fibres innervated by a single alpha motor neuron

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8
Q

What is the neurotransmitter at skeletal muscle neuromuscular junctions?

A

Acetylcholine

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9
Q

A muscle which requires precision more than power (e.g., the hand) has more/fewer muscle fibres per motor unit

A

Fewer (~10)

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10
Q

A muscle which requires power more than precision (e.g., the thigh) has more/fewer muscle fibres per motor unit

A

More (100s - 1000s)

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11
Q

Skeletal muscle fibres usually extend the entire length of muscle. T/F

A

True

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12
Q

Skeletal muscles are attached to bone by…

A

Tendons

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13
Q

A singular muscle fibre (cell) is made up of many…

A

Myofibrils

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14
Q

Myofibrils contain X and Y arranged into Z

A

X - actin
Y - myosin
Z - sarcomeres

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15
Q

The functional unit of skeletal muscle is…

A

the sarcomere

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16
Q

What are the 4 zones of the sarcomere called?

A

A-band
H-zone
M-line
I-band

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17
Q 
Describe each sarcomere zone:
A-band
H-zone
M-line
I-band
A

A-band: area of actin and myosin overlap

H-zone: area in the middle of the A-band where thin filaments don’t reach

M-line: vertical line down the middle of the A-band and H-zone

I-band: initial portion of thin filaments that do not project into A-band i.e., do not overlap thich filaments

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18
Q

How is muscle tension produced?

A

The ATP-dependent sliding of actin filaments over myocin filaments

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19
Q

How does ATP aid skeletal muscle contraction and relaxation?

A

Contraction - broken down into ADP and Pi which energises myosin

Relaxation - releases the actin-myosin cross-bridge and pumps Ca2+ back into the sarcoplasmic reticulum

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20
Q

Why does rigor mortis occur when someone dies?

A

ATP is depleted to Ca2+ can no longer be pumped back into the sarcoplasmic reticulum and so the muscles stay contracted

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21
Q

Describe release of Ca2+ from the sarcoplasmic reticulum in skeletal muscle

A

The surface action potential spreads down the transverse (T)-tubules of the sarcoplasmic reticulum, causing it to release Ca2+ from its lateral sacs

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22
Q

Once myosin is energised by ATP, why is Ca2+ required to form the actin-myosin cross-bridge?

A

Ca2+ binds to troponin and moves the troponin-tropomyosin complex out of the myosin binding site on actin

Energised myosin can then bind to actin and form the cross-bridge

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23
Q

Summarise the process of excitation-contraction coupling in skeletal muscle (7)

A
  1. ACh released across neuromuscular junction
  2. ACh binds and causes an action potential to propegate along the surface membrane
  3. The action potential travels down the T-tubules of the sarcoplasmic reticulum and triggers Ca2+ release from the lateral sacs
  4. Ca2+ binds to troponin on actin filaments, pulling the troponin-tropomyosin complex out of the way to allow the actin-myosin cross bridge to form
  5. Myosin pulls actin towards the centre of the sarcomere using energy from ATP
  6. When there is no longer a local action potential, Ca2+ is actively taken back up by the sarcoplasmic reticulum
  7. With Ca2+ no longer bound to troponin, the troponin-tropomyosin complex blocks the binding site on actin again, and so actin slips back and contraction ends
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24
Q

What 2 factors influence the tension developed by skeletal muscle?

A
  1. The number of muscle fibres/motor units contracting within the muscle
  2. Tension developed by each contracting muscle fibre
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25
Q

How is tension (force of contraction) increased in skeletal muscle?

A

By increasing the frequency of action potential stimulation

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26
Q

The duration of action potential in skeletal muscle is much shorter/longer than the duration of the resulting muscle twitch

A

Shorter

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27
Q

Why does increasing the frequency of action potentials increase muscle tension/force of contraction?

A

When another action potential is fired before the muscle has time to relax from the previous stimulation, the second response is added to the first and a greater muscle tension is developed (= summation of contractions)

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28
Q

What is meant be ‘tetanus’ when referring to skeletal muscle contraction?

A

The maximal sustained contraction caused by twitch summation

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29
Q

What prevents tetanic contraction in cardiac muscle?

A

The long refractory period

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30
Q

Maximum tetanic contraction can be achieved when the muscle is at optimal muscle length (usually resting length). Why is this?

A

This is the optimum length for actin-myosin cross bridge formation

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31
Q

What are the 2 types of skeletal muscle contraction?

A
  • Isotonic contraction

- Isometric contraction

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32
Q

Describe isotonic contraction and when it is used

A
  • Muscle tension remains constant while muscle length changes
  • Used for body movements and moving objects
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33
Q

Describe isometric contraction and when it is used

A
  • Muscle tension develops at constant muscle length

- Used for supporting objects in fixed positions and maintaining body posture

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34
Q

What are the main differences between the 3 different types of skeletal muscle fibres? (3)

A
  • The enzymatic pathways for ATP synthesis
  • Resistance to fatigue (depends on capacity to synthesise ATP)
  • Activity of myosin ATPase (enzyme which controls the speed of the cross-bridge cycle in contraction)
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35
Q

Each motor unit usually contains one/multiple type(s) of muscle fibres

A

One type

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36
Q

What are the 3 pathways for ATP synthesis?

A
  1. Oxidative phosphorylation in mitochondria (main source when O2 present)
  2. Pi from creatine phosphate to ADP (immediate source of energy)
  3. Glycolysis (when O2 not present)
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37
Q

What are the 3 pathways for ATP synthesis?

A
  1. Oxidative phosphorylation in mitochondria (main source when O2 present)
  2. Pi from creatine phosphate to ADP (immediate source of energy)
  3. Glycolysis (when O2 not present)
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38
Q

What are the 3 types of skeletal muscle fibres?

A

Type I - Slow Oxidative

Type IIa - Fast Oxidative

Type IIb - Fast Glycolytic

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39
Q

Describe resistance to fatigue, capacity to synthesise ATP and speed of contraction in the 3 types of skeletal muscle fibres

A

Slow Oxidative Type I - highly resistant to fatigue, high capacity to synthesise ATP, slow in speed

Fast Oxidative Type II1 - medium resistance to fatigue, medium capacity to synthesise ATP, medium speed

Fast Glycolytic Type IIb - low resistance to fatigue, low capacity to synthesise ATP, fast in speed

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40
Q

Describe what activities the 3 different types of skeletal muscle fibres are used for

A

Slow Oxidative Type I - prolonged, low work aerobic activities e.g., maintaining posture, walking

Fast Oxidative Type IIa - aerobic and anaerobic metabolism and prolonged, moderate work activities e.g., jogging

Fast Glycolytic Type IIb - anaerobic metabolism and short term high intensity activities e.g., jumping

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41
Q

Where does the motor unit receive inputs from?

A

The brain and a variety of receptors e.g., withdrawl reflex, stretch reflex

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42
Q

The simplest forms of coordinated movement are called…

A

Reflex actions

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43
Q

What is a reflex action?

A

A stereotyped response to a specific stimulus

44
Q

Describe the stretch reflex arc

A
  • The muscle spindle is the sensory receptor that is activated by muscle stretch
  • Stretching the muscle spindle increases firing in the afferent neurons
  • The afferent neurons synapse in the spinal cord with the alpha motor neurons that innervate the stretched muscle
  • This results in contraction of the stretched muscle
45
Q

Why are tendon reflexes of clinical use?

A

Reflexes help localise a lesion in the nervous system

e.g., a problem with the knee jerk reflex would suggest a problem with spinal nerves L3 and L4 or the femoral nerve

46
Q

What are muscle spindles and where are they found?

A

The sensory receptors for the stretch reflex

They are found within the belly of muscles

47
Q

Muscle spindles are referred to as intrafusal/extrafusal fibres

A

Intrafusal

48
Q

How do muscle spindle fibres run relative to ordinary muscle fibres?

A

They run parallel to ordinary muscle fibres (extrafusal fibres)

49
Q

What are the sensory nerve endings in muscle spindles called?

A

Annulospiral fibres

50
Q

What are the efferent neurons that supply muscle spindles called?

A

Gamma motor neurons

51
Q

Contraction of muscle spindles contributes to the overall strength of muscle contraction. T/F

A

False

52
Q

What 4 factors can lead to impairment of skeletal muscle function?

A
  1. Intrinsic muscle disease
  2. Neuromuscular junction disease
  3. Disease of lower motor neurons which supply the muscle
  4. Disruption of input to motor nerves e.g., upper motor neuron disease
53
Q

List some causes of intrinsic muscle disease (5)

A
  • Congenital myopathies
  • Inflammatory myopathies
  • Non-inflammatory myopathies e.g., fibromyalgia
  • Endocrine myopathies e.g., Cushing syndrome
  • Toxic myopathies e.g., alcohol, statins
54
Q

List 4 symptoms of muscle disease

A
  • Muscle weakness/tiredness
  • Delayed relaxation after voluntary contraction (myotonia)
  • Muscle pain (myalgia)
  • Muscle stiffness
55
Q

List 5 investigations used in neuromuscular disease

A
  • Electromyography (EMG) (electrodes detect the presence of muscle activity)
  • Nerve conduction studies
  • Muscle enzymes e.g., creatine kinase (CK)
  • Inflammatory markers e.g., CRP
  • Muscle biopsy
56
Q

What are the 3 types of joint in the human skeleton?

A

Fibrous
Cartilaginous
Synovial

57
Q

Describe fibrous joints

A
  • Bones are united by fibrous tissue
  • Doesn’t allow any movement (synarthrosis)
  • e.g., bones of the adult skull
58
Q

Describe cartilaginous joints

A
  • Bones are united by cartilage
  • Allow limited movement (amphiarthrosis)
  • E.g., intervertebral discs, pubic symphsis, costochondral joints
59
Q

Describe the structure of a synovial joint

A
  • Bones are separated by a cavity (which contains synovial fluid) and united by a fibrous capsule
  • The articular surfaces of the bones are covered with hyaline cartilage
  • The inner aspect of the fibrous capsule is lined with synovial membrane
60
Q

What makes up the synovial membrane?

A
  • Vascular connective tissue
  • Capillary networks
  • Lymphatics
  • Synovial cells (fibroblasts)
61
Q

How is the synovial fluid produced?

A

By synovial cells (fibroblasts) in the synovial membrane

62
Q

How are synovial joints classified? (2 groups)

A

Simple synovial joint - one pair of articular surfaces e.g., digit joints

Compound synovial joint - more than one pair of articular surfaces e.g., elbow joint

63
Q

As well as the fibrous capsule, what extra-articular structures support the joint? (3)

A

Ligaments
Tendons
Bursae

64
Q

What are the functions of the synovial fluid in the synovial cavity? (3)

A
  • Lubricates the joint so minimises wear-and-tear
  • Reduces friction so facilitates movement
  • Supplies chondrocytes with O2 and nutrients and removes CO2 and waste products (as the articular cartilage is avascular)

-

65
Q

Synovial fluid is static in the synovial cavity. T/F

A

False

The synovial fluid is continuously replenished and absorbed by the synovial membrane

66
Q

Describe the synovial fluid viscosity

A
  • High viscosity due to hyaluronic acid (mucin) produced by synovial cells
  • Viscosity varies with joint movement
67
Q

Describe changes in viscosity and elasticity of synovial fluid during rapid movement (in a normal joint)

A

Viscosity decreases

Elasticity increases

68
Q

Compare the colour, total WCC and polymorph count in normal vs inflammatory vs septic synovial fluid

A

Normal: colourless, WCC <200, PMN count <25

Inflammatory: translucent, WCC 2,000-75,000, PMN count often >50

Septic: opaque, WCC often >100,000, PMN count often >75

69
Q

When might synovial fluid be red?

A
  • Trauma

- Haemorrhagic arthritis

70
Q

What are the 3 main functions of the articular hyaline cartilage?

A
  • Prevents wear-and-tear of joints by providing a low friction, lubricated surface
  • Distributes contact pressure to subchondral bone
  • Composition of the ECM determines the mechanical properties of the cartilage
71
Q

What are the 4 zones of articular cartilage and which one is the largest?

A

(articular surface)
- Superficial zone (10-20%)

  • Middle zone (40-60% -> largest zone)
  • Deep zone (30%)
  • Calcified zone
    (subchondral bone)
72
Q

What are the mechanical properties of water in the articular cartilage?

A
  • Maintains the resilience of the tissue

- Contributes to nutrition and lubrication (most water is found near the articular surface)

73
Q

What are the 4 zones of articular cartilage and which one is the largest?

A

(articular surface)
- Superficial zone (10-20%)

  • Middle zone (40-60% -> largest zone)
  • Deep zone (30%)
  • Calcified zone
    (subchondral bone)
74
Q

Describe the composition of the ECM of the articular cartilage (3)

A

Water (70%)
Collagen (20%)
Proteoglycans (10%)

75
Q

What are the mechanical properties of collagen in the articular cartilage?

A
  • Maintains the cartilage architecture

- Provides tensile stiffness and strength

76
Q

What are the mechanical properties of proteoglycans in the articular cartilage?

A
  • Responsible for the compressive properties associated with weight bearing
77
Q

What proportion of the total cartilage volume is made up of ECM?
What makes up the rest of the <2%?

A

> 98%

Chondrocytes

78
Q

What changes may occur in diseased articular cartilage? (2)

A
  • Changes in the relative amounts of the 3 major articular cartilage components (water, collagen & proteoglycans)
  • If the rate of ECM degradation exceeds the rate of its synthesis
79
Q

List 4 processes that may result in a diseased joint

A
  • Cartilage and synovial deterioration due to ageing and wear-and-tear (e.g., osteoarthritis)
  • Synovial cell inflammation and proliferation (e.g., rheumatoid arthritis)
  • Deposition of salt crystals (e.g., uric acid in gout)
  • Injury and inflammation to periarticular structures (e.g., tendonitis)
80
Q

What effects may be seen in subchondral bone following cartilage wear-and-tear?

A
  • Cyst formation
  • Sclerosis (abnormal hardening of tissue)
  • Osteophyte formation
81
Q

Define pain

A

An unpleasant sensory and emotional experience associated with tissue damage

82
Q

Chronic pain is usually pain that lasts for…

A

> 3 months

83
Q

Name the 4 distinct processes in the physiology of pain

A
  • Transduction
  • Transmission
  • Modulation
  • Perception
84
Q

Describe the 4 processes of pain physiology:

  • Transduction
  • Transmission
  • Modulation
  • Perception
A
  • Transduction: peripheral nociceptor translates noxious stimulus into electrical activity
  • Transmission: pain signal is propagated through the nervous system as nerve impulses
  • Modulation: pain transmission is modified/hindered in the nervous system e.g., by inhibitory neurotransmitters like endogenous opioids
  • Perception: the conscious experience of pain which causes physiological and behavioural responses
85
Q

What are nociceptors?

A

Free nerve endings that are located all over the body and respond to pain caused by noxious stimuli e.g., mechanical, thermal or chemical

86
Q

What type of neurones are nociceptors?

A

Primary sensory afferent

87
Q

What order of neurone is a nociceptor?

A

First order

88
Q

Once the nociceptor has been triggered by a noxious stimulus, what happens in the neuron?

A

Depolarisation occurs and an AP spreads along the axon to second order neurones in the CNS

89
Q

Describe the nociceptive pathway from a peripheral site to the spinal cord and then to the brain

A
  • Free nerve endings (first order neurones) are depolarised and pass information to second order neurones in the spinal cord via neurotransmitters
  • Second order neurones ascend the spinal cord in the anterolateral system
  • The signal is passed to third order neurones in the thalamus
  • Third order neurones relay the information to the primary sensory cortex
90
Q

Name the 2 tracts involved in the anterolateral system that takes second order neurones up the spinal cord.

Briefly state what aspect of pain they are involved in

A
  • Spinothalamic tract (STT) - involved in perception of pain intensity and location
  • Spinoreticular tract (SRT) - involved in autonomic responses to pain, arousal and emotional responses
91
Q

Where are the cell bodies of first, second and third order neurones found?

A

First: dorsal root ganglion of spinal nerves

Second: posterior horn of spinal cord

Third: thalamus

92
Q

Name the 2 subtypes of nociceptors

A

Alpha-delta fibres

C fibres

93
Q

Describe the types of pain that each of the subtypes of nociceptor is involved in

A

A-delta fibres: the immediate sharp pain felt in response to noxious stimuli

C fibres: the second, duller pain remaining after the initial insult

94
Q

Why do A-delta fibres mediate faster pain responses than C fibres?

A

A-delta fibres are myelinated so conduction velocity is fast

C fibres are unmyelinated so conduction velocity is slower

95
Q

Name the 3 types of pain

A
  • Nociceptive
  • Inflammatory
  • Pathological
96
Q

Describe nociceptive pain

A

Nociceptors are provoked by noxious stimuli which are damaging the tissues

97
Q

Describe inflammatory pain

A

The immune system is activated to release mediators by tissue injury or infection

This results in heightened pain sensitivity in the affected area

98
Q

Inflammatory pain causes hyperalgesia and allodynia. What is meant by these terms?

A

Hyperalgesia = heightened pain sensitivity to noxious stimuli

Allodynia = pain sensitivity to innocuous stimuli

99
Q

What are the 2 subtypes of pathological pain?

A

Neuropathic

Dysfunctional

100
Q

Describe neuropathic pathological pain

A

Poorly localised shooting pain or numbness caused by damage to neural tissue

e.g., compression neuropathies, peripheral neuropathies

101
Q

Describe dysfunctional pathological pain

A

Pain with no identifiable damage or inflammation

e.g., fibromyalgia, IBS

102
Q

Which of the 3 types of pain are adaptive and why?

A

Nociceptive pain - it gives a quick warning to remove the noxious stimulus

Inflammatory pain - promotes repair by discouraging physical contact and movement of the affected area

103
Q

Why is pathological pain maladaptive?

A

It occurs in the absence of ongoing noxious stimuli, so is not protective, and does not promote repair

104
Q

What is referred pain?

A

Referred pain = deep or visceral pain felt in an area of skin which is distant from the internal organ where the pain originated

105
Q

Why does referred pain occur?

A

When nociceptive visceral afferents and skin afferents converge on the same spinothalamic neurons at the same spinal level

106
Q 
Where might pain from the...
- Liver
- Gallbladder
- Diaphragm/lungs
- Heart
- Stomach/ pancreas
- Appendix
... be referred to?
A
  • Liver: right side of neck
  • Gallbladder: right shoulder
  • Diaphragm/lungs: left shoulder
  • Heart: left arm and jaw
  • Stomach/ pancreas: centre of abdomen
  • Appendix: umbilicus

LR Musculoskeletal (6 decks)

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