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Musculoskeletal System > Musculoskeletal Growth, Injury and Repair > Flashcards

Musculoskeletal Growth, Injury and Repair Flashcards

1
Q

What are the main anatomical components of a long bone?

A 
Diaphysis - haematopoietic tissues 
Metaphysis - flare at end of shaft
Epiphysis - on joint side of physis
Physis - growth plate
Medullary canal
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2
Q

Why is the diaphysis follow?

A

To increase diameter and strength but keep the bone light

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3
Q

What centres are particularly important in bone growth?

A

Ossification centres

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4
Q

What does cortical bone e.g. the diaphysis resist?

A

Bending and torsion

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5
Q

What are the features of cortical bone?

A

Laid down circumferentially
Less biologically active
Made up of tubes with blood vessels in the middle
Contains osteocytes
Always remodelling without affecting the whole bone

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6
Q

What does cancellous bone e.g. the metaphysis resist?

A

Resists/absorbs compression

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7
Q

What are the features of cancellous bone?

A

Site of longitudinal growth

Very biologically active

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8
Q

What is a fracture?

A

Any break in the structural continuity of bone

May be a crack, break, split, crumpling or buckle

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9
Q

What is the shorthand sign for a fracture?

A

#

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10
Q

What energy is needed to cause normal bones to fracture?

A

High energy transfer - takes a lot of energy in a normal bone to cause a fracture, energy applied in an unexpected way

Or repetitive stress e.g. stress fractures in athletes

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11
Q

What energy is needed to cause abnormal bones to fracture?

A

Only low energy transfer required to fracture an abnormal bone e.g. a bone with osteoporosis, osteomalacia, metastatic tumour, other bone disorders etc.

The older you get, the less energy it takes to cause a fracture

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12
Q

What is the general biological effect of a fracture?

A

Mechanical and structural failure of bone
Disruption of blood supply
Regenerative process - no scar, four stages

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13
Q

What is critical for the progression of fracture healing?

A

Mechanical properties of tissues and there environment

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14
Q

What is involved in stage 1 of the regenerative process following a fracture?

A

Begins immediately after fracture
Haematoma and fibrin clot form immediately
Platelets, PMNs, neutrophils, monocytes and macrophages produce
Lysosomal enzymes
Fibroblasts

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15
Q

What is the role of mesenchymal and osteoprogenitor cells in the regenerative process following a fracture?

A

Transformed endothelial cells from the medullary canal and/or periosteum
Osteogenic induction of cells from muscle and soft tissues

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16
Q

How does angiogenesis occur following a fracture?

A

Oxygen gradient is required in normal bone, this is low in fractures
Macrophages produce angiogenic factors under hypoxic conditions

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17
Q

What can have an effect on stage 1 of the regenerative process?

A

NSAIDs
Loss of haematoma e.g. surgery or open fractures
Extensive tissue damage and poor blood supply

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18
Q

What is stage 2 of the regenerative process following a fracture?

A

Soft callus formation

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19
Q

What is involved in stage 2?

A

Provides some stability of the fracture - fibroblasts produce collagen around the fracture which prevents shortening of the fracture
Angulation can still occur
Continued increase in vascularity

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20
Q

When does stage 2 begin and end?

A

Begins when pain and swelling subside

Lasts until bony fragments are united by cartilage or fibrous tissue

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21
Q

What can have effects on stage 2?

A

Replacing cartilage e.g. DMB
Bone graft
Bone substitutes

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22
Q

What are the features of autogenous cancellous bone graft?

A

Gold standard, best choice for majority of bone graft needs

Osteoconductive or osteoinductive

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23
Q

What are the types of allograft bone grafts?

A 
Cortical
Cancellous
Fresh
Prepared
Structural
Osteoconductive
Non-osteoconductive
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24
Q

What does allograft bone carry a risk of?

A

Disease transmission from donor to recipient

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25
Q

What is stage 3 of the regenerative process following a fracture?

A

Hard callus formation

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26
Q

What is involved in stage 3?

A

Conversion of cartilage to woven bone
Typical long bone fracture - endochondral bone formation and membranous bone formation
Increasing rigidity - secondary bone healing, obvious callus
Although bone is healing it cannot take normal load

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27
Q

What is stage 4 of the regenerative process following a fracture?

A

Bone remodelling

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28
Q

What is involved in stage 4?

A

Conversion of woven bone to lamellar bone
Extra bone is removed as far as possible
Medullary canal is reconstructed
Bone responds to loading characteristics

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29
Q

How does strain affect bone healing?

A

Degree of instability is best expressed as magnitude of strain
If strain is too low, mechanical induction of tissue differentiation fails
If strain is too high, the healing process does not progress to bone formation

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30
Q

What is delayed union?

A

Failure to heal in the expected time

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31
Q

What are the causes of delayed union?

A 
High energy injury 
Distraction 
Instability 
Infection
Steroids 
Immunosuppression
Smoking
Warfarin 
NSAIDs
Ciprofloxacin
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32
Q

What is the effect of smoking on union?

A

50% extension to union

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33
Q

What is non-union?

A

Failure to heal

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34
Q

What are the causes of non-union?

A 
Failure of calcification of fibrocartilage
Usually due to instability 
Abundant callus formation
Pain and tenderness
Persistent fracture line 
Sclerosis
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35
Q

What should be considered in delayed healing?

A

Alternative management:

  • different fixation
  • dynamisation
  • bone grafting
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36
Q

What are the features of ligaments?

A

Dense bands of collagenous tissue
Span a joint
Anchored to the bone at either end
Joint stability through a range of motions
Different portions of the ligament are tensioned at different joint positions

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37
Q

What is the structure of ligaments?

A 
Collagen fibres - type 1 
Fibroblasts - communication 
Sensory fibres - proprioception, stretch and sensory 
Vessels 
Crimping - allows stretch
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38
Q

What is the difference of percentage of collagen, proteoglycans and water, organisation of collagen fibres and shape of fibroblasts between tendons and ligaments?

A

Ligaments have

  • lower percentage of collagen
  • higher percentage of proteoglycans and water
  • less organised collagen fibres and rounder fibroblasts
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39
Q

What causes ligament rupture?

A

When forces applied to the ligament exceed the strength of the ligament - can be complete or incomplete

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40
Q

What needs to be considered in ligament rupture?

A

Effects on the stability of the joint and proprioception loss

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41
Q

What is involved in the healing of ligaments?

A

Haemorrhage
Proliferative phase
Remodelling

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42
Q

What are the features of haemorrhage in the healing of a ligament rupture?

A

Blood clot reabsorbed
Replaced with a heavy cellular infiltrate
Hypertrophic vascular response

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43
Q

What are the features of the proliferative phase of healing of a ligament rupture?

A

Production of scar tissue

Disorganised collagenous connective tissue

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44
Q

What are the features of remodelling in the healing of a ligament rupture?

A

Matrix becomes more ligament-like

Major differences in composition, architecture and function persists

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45
Q

What are the treatment options for ligament injury?

A

Conservative

  • partial
  • no instability
  • poor candidate for surgery

Operative

  • instability
  • expectation e.g. athletes
  • compulsory, multiple e.g. knee dislocation
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46
Q

Where is the motor unit (efferent) located?

A

Anterior horn cell located in the grey matter of the spinal cord
Motor axon and muscle fibres

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47
Q

Where is the sensory unit located?

A

Cell bodies in the posterior root ganglia (i.e. outside the spinal cord)

48
Q

Nerve fibres join to form what?

A

Anterior (ventral) motor roots

Posterior (dorsal) sensory roots

49
Q

What combines to form a spinal nerve?

A

Anterior and posterior roots

50
Q

How do spinal nerves exit the vertebral column?

A

Via an intervertebral foramen

51
Q

What are the features of peripheral nerves?

A

The part of a spinal nerve distal to the nerve roots
Bundles of nerve fibres
Range in diameter from 0.3-22um
Schwann cells form a thin cytoplasmic tube around them
Larger fibres arranged in a multi-layered insulating membrane myelin sheath
Multiple layers of connective tissue surrounding the axons

52
Q

What are peripheral nerves composed of?

A

Highly organised structures comprised of nerve fibres, blood vessels and connective tissue

53
Q

What are axons coated with?

A

Endoneurium

54
Q

What are axons grouped into?

A

Fascicles

55
Q

What are fascicles covered with?

A

Perineurium

56
Q

What are fascicles grouped into?

A

Grouped to form the nerve

57
Q

What is the nerve covered with?

A

Epineurium

58
Q

What are the functions of group IA and IB (A-alpha) afferents?

A

Large motor axons
Muscle stretch
Tension sensory axons

59
Q

What are the functions of group II (A-beta) afferents?

A

Touch, pressure, vibration and joint position sensory axons

60
Q

What are the functions of A-gamma fibres?

A

Gamma efferent motor axons

61
Q

What are the functions of group III (A-delta) afferents?

A

Sharp pain, very light touch and temperature sensation

62
Q

What are the functions of B fibres?

A

Sympathetic preganglionic motor axons

63
Q

What are the functions of group IV (C fibres) afferents?

A

Dull, aching, burning pain and temperature sensation

64
Q

How can peripheral nerves be injured?

A

Compression
Trauma e.g. direct blow, laceration, avulsion
Neurapraxia, axonotmesis, neurotmesis

65
Q

When might peripheral nerves become compressed?

A

Entrapment
Carpal tunnel syndrome (median nerve at wrist)
Sciatica (spinal root by intervertebral disc)
Morton’s neuroma (digital nerve in 2nd or 3rd web space of foot

66
Q

What is neurapraxia?

A

Temporary loss of sensory and motor function due to blockage of nerve conduction - local ischaemia and demyelination, reversible conduction block
Good prognosis

67
Q

What is axonotmesis?

A

Damage to a peripheral nerve where disruption of the axons occurs, but endoneurium, perineurium and epineurium remain intact
Wallerian degeneration follows

68
Q

What causes axonotmesis?

A

Nerve stretched (15% elongation disrupts axons), crushed or a direct blow

69
Q

What causes neurapraxia?

A

Nerve stretched or bruised

70
Q

What is the prognosis of axonotmesis?

A

Fair - sensory recovery often better than motor

Often not returned to normal but returned enough to recognise pain, temperature and sharp and blunt objects

71
Q

What is neurotmesis?

A

Complete nerve division - both the nerve and the nerve sheath are disrupted
Endoneural tubes disrupted so high chance of mis-wiring during regeneration

72
Q

What causes neurotmesis?

A

Laceration or avulsion

73
Q

What is the prognosis of neurotmesis?

A

Poor prognosis

No recovery unless repaired, either by direct suturing or grafting

74
Q

What are closed nerve injuries associated with?

A

Nerve injuries in continuity - classically neuropraxia or axonotmesis

75
Q

When is surgery indicated for closed nerve injuries?

A

After 3 months if no recovery is identified (clinical, electromyography)

76
Q

What is the axonal growth rate?

A

1-3mm/day

77
Q

Give an example of a closed nerve injury

A

Brachial plexus injuries

Radial nerve in humeral fracture

78
Q

What are open nerve injuries usually associated with?

A

Laceration

Frequently related to nerve division - neurotmetic injuries e.g. knives, glass

79
Q

How are open nerve injuries treated?

A

With early surgery

80
Q

At what point does Wallerian degeneration occur?

A

2-3 weeks after the injury

81
Q

What are the sensory clinical features of nerve injury?

A

Dysaesthesiae
Anaesthesia
Hypo/hyper-aesthetic
Paraesthetic

82
Q

What are the motor clinical features of nerve injury?

A 
Paresis or paralysis +/- wasting 
Dry skin (loss of tactile adherence since sudomotor nerve fibres are not stimulating the sweat glands in skin)
83
Q

What are the reflex clinical features of nerve injury?

A

Diminished or absent reflexes

84
Q

What are the features of healing of a nerve injury?

A

Very slow
Starts with initial death of axons distal to site of injury (Wallerian degeneration), then the degradation of the myelin sheath
Proximal axonal budding after about 4 days

85
Q

What is the rate of the regeneration process of a nerve injury?

A

1mm/day

86
Q

What is the first modality to return in the healing of a nerve injury?

A

Pain

87
Q

What does the prognosis for recovery from a nerve injury depend on?

A

Whether the nerve is pure or mixed, and how distal the lesion is
Prognosis is worse with more proximal lesions

88
Q

What sign can be used to monitor recovery?

A

Tinel’s sign - tap over the site of the nerve and parasthesia will be felt as far distally as regeneration has progressed

89
Q

How can nerve injury be assessed and recovery monitored?

A

By electrophysiological nerve conduction studies

90
Q

When is direct repair of a nerve injury indicated?

A

Laceration

No loss of nerve tissue

91
Q

What are the methods of direct repair for a nerve injury?

A

Microscope/Loupes
Bundle repair
Growth factors

92
Q

When is nerve grafting indicated?

A

Nerve loss

Late repair - retraction, sural nerve

93
Q

What is the ‘rule of three’ - surgical timing in traumatic peripheral nerve injury?

A

Immediate surgery within 3 days for clean and sharp injuries

Early surgery within 3 weeks for blunt/contusion injuries

Delayed surgery, performed 3 months after injury, for closed injuries

94
Q

What are the examination findings of an UMN lesion?

A 
Decreased strength 
Increased tone
Increased deep tendon reflexes
Clonus present
Babinski's sign present
Atrophy absent
95
Q

What are the examination findings of a LMN lesion?

A 
Decreased strength 
Decreased tone
Decreased deep tendon reflexes 
Clonus absent 
Babinski's sign absent 
Atrophy present
96
Q

What is the structure of the muscle/tendon composite unit?

A 
Muscle origin from bone 
Muscle belly 
Musculotendinous junction 
Tendon 
Tendinous insertion into bone
97
Q

What is the anatomy of a tendon?

A

Longitudinal arrangement of cells and fibres, orientated along the line of stress
Fascicles of long, narrow, spiralling collagen bundles
Collagen bundles covered by endotenon
Fascicles covered by paratenon
Tendon covered by epitenon

98
Q

What is the blood supply to tendons?

A

Needs to come from outside - rather than running through the middle, this allows tendons to move without damaging blood supply
Viniculum
Fine network of blood vessels in the paratenon

99
Q

How are tendons connected to the tendon sheath?

A

By vincula, synovial lining and fluid

100
Q

What do thickenings of the tendon sheath form?

A

Strong annular pulleys, where tendons have to move round an angle

101
Q

What are the functions of tendons?

A

Flexible and very strong in tension

Movement of the limb in order to enable function

102
Q

What does immobility cause in tendons?

A

Immobility reduces water content and glycosaminoglycan concentration and strength

103
Q

What are the types of tendon injury?

A 
Degeneration 
Inflammation 
Enthesiopathy 
Traction apophysitis
Avulsion +/- bone fragment 
Tear - intrasubstance or musculotendinous 
Laceration/incision
Crush, ischaemia or attrition
Nodules
104
Q

What are the features of degeneration of a tendon?

A

Intra-substance mucoid degeneration
May be swollen, painful, tender or asymptomatic
Possible precursor to rupture
Rheumatoid arthritis should be considered

105
Q

What are the features of inflammation of a tendon?

A

Swollen, tender, hot and red

Positive Finklestein’s test

106
Q

What are the features of enthesiopathy of a tendon?

A

Inflammation at insertion to bone
Usually at muscle origin rather than tendon insertion
Common extensor origin
Tennis elbow - classic presentation

107
Q

What are the features of traction apophysitis?

A

Insertion of patellar tendon into anterior tibial tuberosity
Common in adolescent active boys
Recurrent load
Bone hypertrophies, inflammation occurs
Painful
No cure or treatment other than reducing activity

108
Q

What are the features of avulsion +/- bone fragment?

A

Failure at insertion

Load exceeding failure while muscle contracts

109
Q

What is the treatment for avulsion?

A

Conservative

  • if you can, get tendon ends to re-join
  • limited application
  • retraction tendon

Operative

  • reattachment of tendon, normally through bone
  • fixation bone fragment
110
Q

What causes intrasubstance rupture?

A

Tear

Load exceeds failure strength

111
Q

What is the mechanism of rupture?

A

53% - pushing off with weight bearing forefoot whilst extending knee joint
17% - unexpected dorsiflexion of ankle
10% - violent dorsiflexion of plantar flexed foot

112
Q

What are the features of Achilles tendon rupture?

A

Positive Simmond’s test

Palpable tender gap

113
Q

What is the treatment of tendon rupture?

A

Conservative

  • where ends can be opposed, mobilise, splint/cast
  • where healing will occur

Operative

  • high risk of re-rupture
  • high activity
  • where ends cannot be opposed
114
Q

Why is there no chance of re-joining finger tendons following laceration?

A

Tendon end retracts as soon as it is lacerated

115
Q

What is the treatment of laceration?

A

Repair surgically and early

Musculoskeletal System (40 decks)

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