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Musculoskeletal MBCHB > Physiology > Flashcards

Physiology Flashcards

1
Q

What does it mean if a muscle is striated?

A

alternating dark bands and light bands

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2
Q

Describe skeletal muscle

A

Striated muscle under voluntary control - somatic nervous system

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3
Q

Describe cardiac muscle

A

Striated muscle under involuntary control - autonomic nervous system

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4
Q

Describe smooth muscle

A

Non-striated muscle under involuntary control - autonomic nervous system

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5
Q

Describe the initiation and propagation of contraction in skeletal muscle

A

Neurogenic initiation of contraction
Motor units
Neuromuscular junction present
No gap junctions present

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6
Q

Describe the initiation and propagation of contraction in cardiac muscle

A

Myogenic initiation of contraction
No neuromuscular junction
Gap junctions present

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7
Q

What are the functions of skeletal muscle?

A
  • Maintenance of posture
  • Purposeful movement in relation to external environment
  • Respiratory movement
  • Heat production
  • Contribute to whole body metabolism
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8
Q

What is the motor unit of skeletal muscle?

A

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

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9
Q

How does the number of muscle fibres per motor unit vary in skeletal muscle?

A
  • Muscles which serve fine movements (e.g. external eye muscles, muscles of facial expression, intrinsic hand muscles) have fewer fibres per motor unit - precision is more important than power
  • Muscles (e.g. thigh muscles) where power is more important than precision will have hundreds to thousands of fibres per motor unit
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10
Q

Explain the organisation of muscle fibres.

A
  • Skeletal muscle consists of parallel muscle fibres (skeletal muscle cells) bundled by connective tissue
  • Skeletal muscle fibres usually extend the entire length of the muscle
  • Skeletal muscles are usually attached to skeleton by tendons
  • Bones, muscles and joints form lever systems that allow a range of body movements
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11
Q

What are myofibrils?

A

specialised intracellular structures

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12
Q

Describe the structure of myofibrils.

A

Myofibrils have alternating segments of thick (myocin - darker) and thin (actin - lighter) protein filaments

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13
Q

What are sarcomeres?

A

Within each myofibril actin and myocin are arranged into sarcomeres - these are the functional units of the muscle

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14
Q

What is a functional unit of an organ?

A

The functional unit of an organ is the smallest component of performing all the functions of the organ

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15
Q

Where are sarcomeres found?

A

found between two Z lines - connect the thin filaments of 2 adjoining sarcomeres

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16
Q

What are the 4 zones in a sarcomere?

A

A band
H zone
M line
I band

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17
Q

What is the A band?

A

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

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18
Q

What is the H zone?

A

lighter area within middle of A-band where thin filaments don’t reach

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19
Q

What is the M line?

A

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

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20
Q

What is the I band?

A

consists of remaining potion of thin filaments that do not project in the A-band

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21
Q

What is the sliding filament theory?

A
  • muscle tension is produced by sliding of actin filaments on myocin filaments
    • ATP required for contraction (powers cross bridges) and relaxation (release of cross bridges and to pump Ca2+ back into SR)
    • Ca2+ required for cross bridge formation
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22
Q

Describe excitation-contraction coupling?

A

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

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23
Q

What is the role of calcium in excitation-contraction coupling?

A

Ca2+ is the link between excitation and contraction - in skeletal muscle fibres Ca2+ is released from the lateral sacs of the sarcoplasmic reticulum when the surface action potential spreads down the T-tubules

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24
Q

What are T-Tubules?

A

extensions of the surface membrane that dip into the muscle fibre

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25
Q

What are the stages of excitation-contraction coupling?

A
  1. ACh released by axon of motor neuron, crosses cleft and binds to receptors on motor end plate (no continuity of cytoplasm between nerve and skeletal muscle cells)
  2. Action potential generated in response to ACh is propagated across surface membrane and down T-tubules of muscle cell
  3. Action potential in T-tubules triggers Ca2+ release from sarcoplasmic reticulum
  4. Ca2+ ions released from lateral sacs bind to troponin on actin filaments - leads to tropomyosin being physically moved aside to uncover cross-bridge binding sites on actin
  5. Myosin across bridges attach to actin and bend, pulling actin filaments towards the centre of sacromere - energy is provided by ATP
  6. Ca2+ is actively taken up by SR when there is no longer action potential
  7. With Ca2+ no longer bound to troponin, tropomyosin slips back into its blocking position over binding sites on actin, contraction ends, actin passively slides back to resting position
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26
Q

What are the factors determining graduation of muscle tension?

A

Number of muscle fibres contracting within the muscle
Tension developed by each contracting muscle fibre

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27
Q

How does the number of muscle fibres contracting within the muscle determine graduation of muscle tension?

A
  • A stronger contraction could be achieved by stimulation of more motor units - motor unit recruitment
  • Asynchronous motor unit recruitment during submaximal contractions help prevent muscle fatigue
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28
Q

How does the tension developed by each contracting muscle fibre determine graduation of muscle tension?

A

Depends on:

  • Frequency of stimulation and summation of contractions (see below)
  • Length of muscle fibre at the onset of contraction
  • Thickness of muscle fibre
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29
Q

What is a twitch?

A

If the skeletal muscle is stimulated once, a single contraction called a twitch is produced
A single twitch produces little tension and is not useful in bringing about meaningful skeletal muscle activity

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30
Q

What is tetanus?

A
  • If a muscle fibre is stimulated so rapidly that it does not have an opportunity to relaxed at all between stimuli, a maximal sustained contraction (tetanus) occurs
    • Cardiac muscle cannot be tetanised - prevented by the long refractory period of cardiac muscle
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31
Q

What is isotonic contraction?

A
  • muscle tension remains constant as the muscle length changes
    • Used for body movements and moving objects
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32
Q

What is isometric contraction?

A
  • muscle tension develops at constant muscle length
    • Used for supporting objects in fixed positions and maintaining body posture
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33
Q

Describe type I skeletal muscle fibres.

A

(aka slow-twitch fibres) are used mainly for prolonged relatively low work aerobic activities e.g. maintenance of posture, walking

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34
Q

Describe type IIa skeletal muscle fibres.

A

(aka intermediate-twitch fibres) use both aerobic and anaerobic metabolism and are useful in prolonged relatively moderate work activities e.g. jogging

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35
Q

Describe type IIb skeletal muscle fibres

A

(aka fast-twitch fibres) use anaerobic metabolism and are mainly used for short-term high intensity activities e.g. jumping

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36
Q

What are the metabolic pathways that supply ATP in muscle fibres?

A
  • Transfer of a high-energy phosphage from creatine phosphate to ADP - immediate source of ATP
  • Oxidative phosphorylation - main source when O2 present
  • Glycolysis - main source when O2 not present
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37
Q

Explain the stretch reflex.

A
  • The stretch reflex is the simplest monosynaptic spinal reflex
  • It serves as a negative feedback mechanism that resists passive change in muscle length to maintain optimal resting length of muscle
  • Helps to maintain posture e.g. while walking
  • The sensory receptor is the muscle spindle and 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 (efferent limb of the stretch reflex) that innervate the stretched muscle
  • Activation of the reflex results in contraction of the stretched muscle
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38
Q

How can a stretch reflex be tested?

A
  • It can be elicited by tapping the muscle tendon with a rubber hammer
    • This rapidly stretches the muscle (e.g. quadriceps femoris in knee jerk) → contraction
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39
Q

What are muscle spindles?

A

a collection of specialised muscle fibres which act as sensory receptors for the stretch reflex

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40
Q

Where are muscle spindles found?

A
  • Muscle spindles are found within the belly of muscles and run parallel to ordinary muscle fibres
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41
Q

What is the muscles spindles nerve supply?

A
  • Muscle spindles have their own efferent (motor) nerve supply
    • The efferent neurons that supply muscle spindles are called 𝛾-motor neurons
    • The 𝛾-motor neurons adjust the level of tension in the muscle spindles to maintain their sensitivity when the muscle shortens during contraction
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42
Q

What are the functions of joints?

A
  • Structural support
  • Purposeful movement
    • Stress distribution
    • Confer stability - shape of articular component, ligaments, synovial fluid (acts as an adhesive seal)
    • Joint lubrication - cartilage interstitial fluid, synovium-derived hyaluronic acid (mucin - polymer of dissacharides), synovium-derived lubricin (glycoprotein)
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43
Q

What are the different types of joints?

A
  • Synovial (diarthrosis)
  • Fibrous (synarthrosis): bones united by fibrous tissue, doesn’t usually allow any movement
    • Examples are the bones of the skull in adults
  • Cartilaginous (amphiarthrosis): bones united by cartilage, allow limited movement
    • Examples are the IV discs, pubic symphysis, part of the sacroiliac joints, costochondral joins
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44
Q

Describe synovial joints?

A

Bones are separated by a cavity (containing synovial fluid) and united by a capsule (and other extra-articular structures e.g. ligaments, tendons and bursae)

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45
Q

What is the synovial membrane?

A

lines the inner aspect of the fibrous capsule
Contains synovial cells (fibroblasts) which produces the synovial fluid

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46
Q

Describe simple synovial joint?

A

one pair of articular surfaces e.g. metacarpophalangeal joint

47
Q

Describe a compound synovial joint?

A

more than one pair of articular surfaces e.g. elbow joint

48
Q

What is synovial fluid?

A
  • Fills the joint cavity (volume <3.5 ml in adult knee)
  • The synovial fluid is continuously replenished by the synovial membrane i.e. not a static pool
  • It has a high viscosity - mainly due to the presence of hyaluronic acid (mucin) produced by the synovial cells
49
Q

Describe the variability of viscosity and elasticity of the synovial fluid.

A
  • The viscosity and elasticity of the synovial fluid varies with joint movement
    • Rapid movement is associated with decreased viscosity and increased elasticity
    • These properties of synovial fluid become defective in a diseased joint e.g. in osteoarthritis
50
Q

Describe the appearance of normal synovial fluid.

A
  • The normal synovial fluid is clear and colourless
  • Normally the synovial fluid contains few cells (mainly mononuclear leucocytes)
    • Normally <200 WBC/mm3 of which polymorphs are usually <25/mm3
51
Q

What may change to the synovial fluid in septic arthritis?

A

Synovial fluid WBC increases in inflammatory and septic arthritis

52
Q

When does synovial fluid turn red?

A

in traumatic synovial tap and in haemorrhagic arthritis

53
Q

What is the function of synovial fluid?

A
  • Lubricates joint
  • Facilitates joint movement - reduces friction
  • Helps minimise wear-and-tear of joints through efficient lubrication
  • Aids in the nutrition of articular chondrocytes
  • Supplies the chondrocytes with O2 and nutrients and removes CO2 and waste products (articular cartilage is avascular)
54
Q

What is the function of articular cartilage?

A
  • Provides a low friction lubricated gliding surface which helps prevent wear-and-tear of joints
  • Distributes contact pressure to subchondral bone
  • The cartilage composition of the cartilage ECM and the interaction between the fluid and solid phase of the cartilage plays a significant role in determining the mechanical properties of cartilage
55
Q

Describe the structure of articular cartilage

A
  • The articular cartilage is usually hyaline
  • It is elastic and has sponge-like property
  • The zones differ in organisation of collagen fibres and relative content of cartilage components
56
Q

What components make up extra-cellular matrix?

A

Water (70%) - maintains the resiliency of the tissue and contributes to the nutrition and lubrication system
Collagen (20%) - mainly type II (elastic)
Proteoglycans (10%) - responsible for the compressive properties associated with load bearing (act like ‘balloons’)

57
Q

How is the ECM synthesised?

A
  • Synthesized, organised and degraded by chondrocytes - usually constitutes <2% of the total cartilage volume
  • The articular cartilage is avascular and the chondrocytes receive nutrients and O2 via the synovial fluid
58
Q

What may go wrong in a joint?

A
  • Cartilage and synovial fluid decomposition and function deteriorate with age and repeated wear and tear → osteoarthritis
  • Synovial fluid proliferation and inflammation → rheumatoid arthritis
  • Deposition of salt crystals e.g. uric acid → gouty arthritis
  • Injury and inflammation to periarticular structures can cause soft tissue rheumatism e.g. injury to the tendon causes tendonitis
59
Q

How is skeletal muscle innervated?

A

Skeletal muscle is innervated by fast conducting ⍺-motoneurones with myelinated axons and cell bodies in the spinal cord or brain stem

60
Q

How is an individual muscle fibre innervated?

A

Near the muscle, the axon divides into unmyelinated branches that innervate an individual muscle fibre

61
Q

How is a chemical synapse created within a muscle membrane?

A

Individual branches further divide into multiple fine branches that end in a terminal bouton - forms a chemical synapse with the muscle membrane at the neuromuscular junction

62
Q

How is acetylcholine released in skeletal muscle?

A

Action potentials arising in the cell body are conducted via the axon to the boutons, causing the release of ACh

63
Q

What are the key features of the skeletal neuromuscular junction?

A

terminal bouton (and surrounding Schwann cell), synaptic vesicles, synaptic cleft, end plate region (sarcolemma)

64
Q

How is acetylcholine synthesised and stored?

A
  • Choline transporter takes choline into pre-synaptic terminal (symport with Na+)
  • ACh is synthesised from choline and acetyl CoA by choline acetyltransferase
  • ACh is concentrated in vesicles by the vesicular ACh transporter where they are stored until an action potential arrives
65
Q

Describe a nicotinic ACh receptor

A
  • Two ACh molecules activate each nicotinic ACh receptor (nAChR)
  • nAChrs are pentamers of glycoprotein subunits surrounding a central cation selective pore
  • Pore contains a gate that opens when ACh binds to the exterior of the receptor
66
Q

What happens when a nicotinic ACh receptor is activated?

A
  • When the gate is open there is simultaneous Na+ influx and K+ efflux
  • Because the driving force for Na+ is greater than for K+ at resting membrane potential influx of Na+ is greater than efflux of K+ - rapid depolarising end plate potential is generated by the simultaneous opening of many nAChRs
67
Q

Explain the electrical response that initiates contraction.

A
  • Many miniature end plate potentials summate to produce the endplate potential - a graded response
  • An endplate potential that exceeds the threshold triggers the opening of voltage activated Na+ channels around the endplate - causes an ‘all or none’ propagated action potential that initiates contraction (normally always occurs)
68
Q

Why are voltage-activated Na+ channels required?

A
  • If an endplate had only nAChr receptors, the endplate potential would wane as it spreads from the endplate - no contraction
  • Having a muscle fibre with voltage activated Na+ channels means that the action potential propagates from the endplate over the length of the muscle fibre - contraction
69
Q

What does the release of calcium cause?

A

The release of Ca2+ causes contraction by interacting with troponin associated with the myofibrils

70
Q

Explain the stages of termination of the action of ACh.

A
  • Acetylcholinesterase (AChE) at the endplate membrane hydrolyses ACh into choline and acetate
  • Choline is taken up by the choline transporter
  • Acetate diffuses from the synaptic cleft
  • AChE is very efficient - hydrolyses some ACh molecules even prior to ACh binding to receptors, once unbinding occurs virtually all ACh molecules are hydrolysed
    • Limits rebinding and means the endplate potential is terminated within a few miliseconds
71
Q

What causes neuromytonia?

A
  • In the acquired form (most common, autoimmune) - antibodies against voltage-activated K+ channels in the motor neurone disrupt functioning resulting in hyperexcitability and repetitive firing
    • Repetitive firing → prolonged endplate potential and repetitive potential discharge in skeletal muscle fibres
72
Q

What symptoms are related to neuromytonia?

A

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

73
Q

How is neuromytonia treated?

A

Drug treatment includes anti-convulsants (e.g. carbamazepine, phenytoin) which block voltage-activated Na+ channels

74
Q

What other condition is Lambert-Eaton Myasthenic Syndrome associated with?

A

Very rare, associated with small cell carcinoma of the lung

75
Q

What symptom is characteristic of Lambert-Eaton Myasthenic Syndrome?

A
  • Characterised by muscle weakness in the limbs
    • May transiently improve upon exertion
76
Q

What causes Lambert-Eaton Myasthenic Syndrome?

A

Autoimmune origin in many cases - antibodies against voltage activated Ca2+ channels in the motor neuron terminal result in reduced Ca2+ entry in response to depolarisation → reduced ACh release

77
Q

What is the treatment for Lambert-Eaton Myasthenic Syndrome?

A

Drug treatment includes anticholinesterases (e.g. pyridostigmine) which increases duration of ACh in the synaptic cleft and potassium channel blockers (e.g. 3,4-diaminopyridine) which increase the release of ACh by prolonging the action potential in the motoneurone terminal

78
Q

What symptoms are characteristic of Myasthenia Gravis?

A

Characterized by progressively increasing muscle weakness during periods of activity (fatiguability)

79
Q

What is the cause of myasthenia gravis?

A

Autoimmune origin in many cases - autoantibodies against nAChr in the endplate results in reduction in the number of functional channels → amplitude of endplate potential decreases

80
Q

What is the treatment for myasthenia gravis?

A

Drug treatment includes anticholinesterases (e.g. pyridostigmine) which increase the concentration of ACh in the synaptic cleft, and a variety of immunosuppressant agents (e.g. azathioprine)

81
Q

What is botulinum toxin? and how does it work?

A
  • Extremely potent exotoxin that acts at motor neurone terminals to irreversibly inhibit ACh release
  • Enters presynaptic terminals to enzymatically modify proteins involved in the docking of vesicles containing ACh to the presynaptic membrane, which prevents exocytosis
82
Q

What is the treatment for botulinum toxin?

A
  • High death rate, recovery takes weeks
  • Anti-cholinesterases are ineffective as therapy
  • Low dose botulinum haemaglutin complex can be administered IM to treat overactive muscles (dystonias) and also ‘botox’ for wrinkles
83
Q

How is calcium homeostasis regulated?

A

regulated by the effects of PTH and 1,25-dihydroxyvitamin D3 on the gut, kidney and bone

84
Q

Where are there calcium sensing receptors?

A

In the parathyroid glands, kidney and brain

85
Q

How does PTH regulate calcium?

A

PTH increases plasma calcium through many mechanisms, including increasing osteoclastic activity in bone and increasing intestinal absorption of calcium

86
Q

What is transduction?

A

translation of noxious stimulus into electrical activity at the peripheral nociceptor

87
Q

What is transmission (pain)?

A

propagation of pain signal as nerve impulses travel through the nervous system

88
Q

Explain the modulation phase in the process of pain?

A

modification/hindering of pain transmission in the nervous system e.g. by inhibitory neurotransmitters like endogenous opioids

89
Q

Explain the perception phase in the process of pain.

A

conscious experience of pain, causes physiological and behavioural responses

90
Q

What are nociceptors?

A

Nociceptors are first order neurones that relay information to second order neurones in the CNS by chemical synaptic transmission

91
Q

What are nociceptors?

A

Nociceptors are first order neurones that relay information to second order neurones in the CNS by chemical synaptic transmission

92
Q

How are nociceptors activated?

A

normally activated by intense noxious stimuli (mechanical, thermal or chemical)

93
Q

How do second order neurones ascend the spinal cord?

A
  • ascend the spinal cord in the anterolateral system (terminate in the thalamus) comprising mainly:
    • The spinothalamic tract (STT) - involved in pain perception (location, intensity)
    • The spinoreticular tract (SRT) - involved in autonomic responses to pain, arousal, emotional responses, fear of pain
94
Q

How is information passed onto third order neurones?

A

From the thalamus, sensory information is relayed (third order neurones) to the primary sensory cortex

95
Q

Describe Aδ-fibres?

A

mechanical/thermal nociceptors that are thinly myelinated, respond to noxious/mechanical and thermal stimuli; mediate ‘first’, or fast, pain

96
Q

Describe C-fibres.

A

nociceptors that are unmyelinated, collectively respond to all noxious stimuli (polymodal); mediate ‘second’ or slow pain

97
Q

What is nociceptive pain?

A

represents normal response to injury of tissues by noxious stimuli
Nociceptive pain is adaptive - functions as an early warning physiological protective system to detect and avoid noxious stimuli

98
Q

How is nociceptive pain stimulated?

A

Provoked by intense stimulation of nociceptors by noxious stimuli (mechanical, chemical, thermal)

99
Q

What is inflammatory pain?

A

caused by activation of the immune system by tissue injury or infection

100
Q

How does inflammatory pain work?

A
  • Causes heightened pain sensitivity to noxious stimuli (hyperalgesia) and pain sensitivity to innocuous stimuli (allodynia)
    • This discourages physical contact (with the affected part) and discourages movement (e.g. of a joint) - inflammatory pain is adaptive as it promotes repair until healing occurs
101
Q

How is inflammatory pain stimulated?

A

Pain is activated by a variety of mediators released at the site of inflammation by leukocytes, vascular endothelium and tissue resident mast cells

102
Q

What is neuropathic pain?

A

caused by damage to neural tissue

103
Q

What are examples of neuropathic pain?

A

compression neuropathies, peripheral neuropathies, central pain (following stroke or spinal injury) posthereptic neuralgia, trigeminal neuralgia, phantom limb

104
Q

How is neuropathic pain felt?

A
  • Can be percieved as burning, shooting, numbness, pins and needles
  • May be less localised
105
Q

What is dysfunctional pain?

A

in dysfunctional pain there is no identifiable damage or inflammation

106
Q

What are examples of dysfunctional pain?

A

fibromyalgia, IBS, tension headache, temporomandibular joint disease, interstitial cystitis

107
Q

How can dysfunctional pain be treated?

A
  • Simple analgesics usually not very effective in pathological pain
    • Sometimes treated by drugs not originally developed for pain e.g. antidepressants or antileptics
108
Q

What is referred pain?

A

pain developed in one part of the body felt in another structure away from the place of its development

109
Q

How is referred pain felt?

A

Deep pain or visceral pain

110
Q

What causes referred pain?

A

Referred pain is caused by convergence of nociceptive visceral and skin afferents upon the same spinothalamic level

111
Q

When does primary bone healing occur?

A

This process occurs where there is minimal fracture gap (less than about 1mm) and the bone simply bridges the gap with new bone from osteoblasts

112
Q

What is secondary bone healing?

A
  • In the majority of fractures, there is a gap at the fracture site which needs to be filled temporarily to act as a scaffold for new bone to be laid down
  • This is known as secondary bone healing and involves an inflammatory response with recruitment of pluropotential stem cells which differentiate into different cells during the healing process
113
Q

Describe the process of secondary bone healing.

A
  1. Fracture occurs
  2. Haematoma occurs with inflammation from damaged tissues
  3. Macrophages and osteoclasts remove debris and resorb the bone ends
  4. Granulation tissue forms from fibroblasts and new blood vessels
  5. Chondroblasts form cartilage (soft callus)
    1. Usually formed by the 2nd-3rd week
  6. Osteoblasts lay down bone matrix (collagen type 1) - enchondral ossification
  7. Calcium mineralisation produces immature woven bone (hard callus)
    1. Takes approximately 6-12 weeks
  8. Remodelling occurs with organization along lines of stress into lamellar bone
114
Q

What are the requirements for bone healing?

A
  • Secondary bone healing requires a good blood supply for oxygen, nutrients and stem cells and also requires a little movement or stress (compression or tension)
  • Lack of blood supply, no movement (internal fixation with fracture gap), too big a fracture gap or tissue trapped in the fracture gap may result in an atrophic non‐union
  • Smoking may severely impair fracture healing due to vasospasm whilst vascular disease, chronic ill health and malnutrition will also impair fracture healing
  • Hypertrophic non-unions occur due to excessive movement at the fracture site with abundant hard callus formation but too much movement give the fracture chance to bridge the gap

Musculoskeletal MBCHB (21 decks)

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