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Year 3 > Musculoskeletal Growth/Injury and Repair > Flashcards

Musculoskeletal Growth/Injury and Repair Flashcards

1
Q

what are ligaments?

A

dense bands of collagenous tissue that span a joint. they are anchored to bone at both ends

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2
Q

what do ligaments do?

A

aid joint stability through a range of motion

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3
Q

what are ligaments made from?

A

type 1 collagen fibres

fibroblasts

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4
Q

what kind of sensory fibres are found in ligaments?

A

proprioception
stretch
sensory

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5
Q

what allows ligaments to stretch?

A

crimping

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6
Q

compared to tendons, ligaments have: % collagen, proteoglycans, water, collagen fibres, fibroblasts

A

less collage
more proteoglycans and water
less organised collagen fibres
rounder fibroblass

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7
Q

when do ligaments rupture?

A

forces that exceed the strength of the liagment

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8
Q

what determines how much a ligament is ingjured

A

whether the forcewas expected or not

rate of load

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9
Q

what are the stages of ligament healing?

A

haemorrhage
proliferative phase
remodelling

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10
Q

healing of ligaments: haemorrhage phase

A

blood clot
reabsorbed
replaced with a heavy cellular infiltrate
hypertrophic vascular response

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11
Q

healing of ligaments: proliferative phase

A

production of scar tissue

disorganised collagenous connective tissue

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12
Q

healing of ligaments: remodelling phase

A

matrix becomes more ligament like

major differences in composition, architecture and function persist

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13
Q

when would you treat ligaments conservatively?

A

partial
no instability
poor candidate for surgery

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14
Q

when would you treat ligaments operative?

A

instability
expectation - sportsmen
compulsory- multiple

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15
Q

describe the process of growth and ossification with a diagram

A

see notes

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16
Q

where is cortical bone found?

A

diaphysis

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17
Q

where is cancellous bone?

A

metaphysis

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18
Q

features of cortical bone

A

resists bending and torsion
laid down circumferentially
less biologically active

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19
Q

features of cancellous bone

A

resists/absorbs compression
site of longitudinal growth
v biologically active

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20
Q

what are the stages in bone healing?

A

inflammation
soft callus
hard callus
bone remodelling

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21
Q

stages in bone healing: inflammation

A

immediately after fracture
haematoma and fibrin clot forms
mesenchymal and osteoprogenitor cells are transformed endothelial cells from medullary canal and/ir periosteum
osteogenic induction of cells from muscle and soft tissues
low oxygen gradient required for angiogenesis

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22
Q

what cells are involved in the inflammatory stage of bone healing?

A 
platelets
PMN's 
neutrophils
monocytes
macrophages
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23
Q

in bone healing, what are the by products of cell dealth cleared up by?

A

lysosomal enzymes

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24
Q

what produces angiogenic factors under hypoxic conditions?

A

macrophages

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25
Q

what factors could alter the first stage in bone healing?

A

NSAIDs
loss of haematoma (open fractures, surgery)
extensive tissue damage resulting in poor blood supply

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26
Q

what platelet concentrates are implicated in the inflammatory stage of bone healing?

A

platelet derived growth factor PDGF
transforming growth factor beta TGF-b
insulin like growth factor IGF
vascular endothelial growth factor VEGF

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27
Q

stages in bone healing: soft callus

A 
begins when pain and swelling subside
lasts undil bony fragments are united by cartilage or fibrous tissue
some stability of the fracture
angulation can still occur
increased vascularity
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28
Q

what can affect the soft callus formation?

A

replacing cartilage with demineralised bone matrix

placement of bone grafts

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29
Q

what would the best autogenous cancellous bone graft have?

A

osteoconductive
osteoinductive
best choice

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30
Q

what is an allograft bone?

A 
cortical
cancellous
fresh
prepared
structural
osteoconductive
not osteoinductive
creeping substitution
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31
Q

what risk is there with bone allografts?

A

disease transmission

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32
Q

stages in bone healing: hard callus

A

conversion of cartilage to woven bone
in typical long bones there is endochondral and membranous bone formation
increasing rigidity and secondary bone remodelling
can be seen on xray

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33
Q

stages in bone healing: bone remodelling

A

woven bone converted to lamellar bone
medullary canal reconstituted
Wolff’s law applies

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34
Q

what is delayed union?

A

when a fracture fails to heal in the expected time

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35
Q

causes of delayed union

A
  1. High energy injury
  2. Distraction results in increased osteogenic jumping
  3. Instability
  4. Infection
  5. Steroids
  6. Immune suppressants
  7. Smoking
  8. Warfarin
  9. NSAID
  10. Ciprofloxacin
  11. Failure of calcification fibrocartilage
  12. Instability – excessive osteoclasis
  13. Abundant callus formation
  14. Pain and tenderness
  15. Persistent fracture line sclerosis
36
Q

in delayed union how could you treat it?

A

different fixation
dynamisation
bone grafting

37
Q

what is a tendon?

A 
muscle origin from bone
muscle belly
musculotendinous juntion
tendon (? sesamoid bone, ? tendon sheath)
tendinous insertion into bone
38
Q

structure of tendons

A

longitudinal arragement of cells (tenocytes) and fibres (type 1 collagen)
long narrow spiralling of collagen bundles known as fasicles

39
Q

what are collagen bundles covered by? (Tendons)

A

endotenon

40
Q

what are tendon fascicles covered by?

A

paratenon

41
Q

what is a tendon covered with?

A

epitenon

42
Q

describe a tendon sheath

A

Tendons are connected to the sheath by vincula and there is a synovial lining with fluid giving lubrication and nutrition. Thickenings of the tendon sheath form strong annular pulleys. Tendons are flexible structures that are very strong when tensed.

43
Q

what effect does immobility have on tendons?

A

reduces water content and glycosaminoglycan concentration and strength

44
Q

what kind of injuries affect tendons?

A 
degeneration
inflammation
enthesiopathy
traction apophysitis
avulsion +/- bone fragment
tear - intrasubstance/musculotendinous junction
laceration
crush
ischaemia
attrition
nodules
45
Q

injuries to tendons: degenration

A

intrasubstance mucoid degeneration
may be swollen, painful, tender, may be asymptomatic
?precursors to rupture

46
Q

what tendon commonly degenerates?

A

achilles

47
Q

injuries to tendons: inflammation

A

de Quervain’s stenosing tenovaginitis
tendons of EPB and APL passing through common tendon sheath at radial aspect of wrist
swollen, tender, hot, red
positive Finklestein’s test

48
Q

injuries to tendons: enthesiopathy

A

inflammation at insertion to bone muscle/tendon

usually at muscle origin rather than tendon insertion e.g. lateral humeral epicondylitis (Tennis elbow)

49
Q

give an example of enthesiopathy in a ligament

A

plantar fasciitis

50
Q

injuries to tendons: traction apophysitis

A 
Osgood Schlatter's disease
insertion of patellar tendon into anterior tibial tuberosity
adolescent active boys
recurrent load
inflammation
51
Q

injuries to tendons: avulsion treatment

A

conservative - limited application, retraction tendon

operative - reattchment tendon through bone, fixation bone fragment

52
Q

injuries to tendons: intrasubstance rupture

A 
achilles
load exceeds failure strength
mechanism of rupture:
Pushing off with weight bearing forefoot whilst extending knee joint (53%) e.g. sprint starts or jumping movements
▪ Unexpected dorsiflexion of ankle (17%) e.g. slipping into hole
▪ Violent dorsiflexion of plantar flexed foot (10%) e.g. fall from height
o Treatment
▪ Conservative
• Where ends can be opposed
o Mobilise (partial rupture) e.g. medial ligament of knee
o Splint
Figure 5 Pulley System in Digits
• Where healing will occur
o Not intraarticular
▪ Operative
• High risk rerupture
• High activity
• Ends cannot be opposed
53
Q

injuries to tendons: tear at musculotendinous junction

A

medial head of gastrocnemius at musculotendinous junction with achilles
mis called plantaris syndrome
often partial

54
Q

injuries to tendons: laceration

A 
E.g. finger flexors (FDS and FDP)
▪ Common
▪ Males > females
▪ Young adults
▪ Repair surgically and early but beware old injuries
▪ Technically challenging
55
Q

describe a peripheral nerve

A

This is the part of a spinal nerve distal to the roots. They are bundles of nerve fibres that range in diameter from 0.3-22𝜇m. Schwann cells form a thin cytoplasmic tube around the nerves. Larger fibres are found in multi-layered insulating membranes known as myelin sheaths. There are multiple layers of connective tissue surrounding axons.
A peripheral nerve is a highly organised structure comprised of nerve fibres, blood vessels and connective tissue. Axons are coated with endoneurium and grouped into fasicles covered with perineurium and grouped into nerves covered with epineurium.

56
Q

function of Aa nerve fibres (IA, IB)

A

large motor axons
muscle stretch
tension sensory axons

57
Q

function of Ab nerve fibres (II)

A 
touch
pressure
vibration
joint proprioception
sensory axons
58
Q

function of Ay nerve fibres

A

efferent motor axons

59
Q

function of Ad nerve fibres (III)

A

sharp pain
very light touch
temperature

60
Q

function of B nerve fibres

A

sympathetic preganglionic motor axons

61
Q

function of C nerve fibres

A

dull, aching,burning pain

temperature

62
Q

types of injury to nerves

A

compression

trauma

63
Q

examples of nerve compression injury

A

o Entrapment
o Carpal tunnel syndrome – median nerve at wrist
o Sciatica – spinal root by IV disc
o Morton’s neuroma – digital neuroma in 2nd or 3rd web space of forefoot

64
Q

examples of direct nerve trauma

A

blow

laceration

65
Q

examples of indirect nerve trauma

A

avulsion

traction

66
Q

what can nerve trauma result in?

A

neurpraxia
axonotmesis
neurotmesis

67
Q

describe neurapraxia

A

▪ Nerve in continuity
▪ Stretched (8% will damage microcirculation) or bruised
▪ Revisable conduction block – local ischaemia and demyelination
▪ Prognosis good (weeks or months)

68
Q

describe axonotmesis

A

▪ Endoneurium intact (tube in continuity) but disruption of axons; more severe injury
▪ Stretched ++ (15% elongation disrupts axons) or crushed or direct blow
▪ Wallerian degeneration follows
▪ Prognosis fair
• Sensory recovery better than motor
• Often not normal but enough to recognise pain, hot, cold, sharp, blunt

69
Q

describe neurotmesis

A

Complete nerve division
▪ Laceration or avulsion
▪ No recovery unless repaired by direct suturing or grafting
▪ Endoneural tubes disrupted so high chance of miswiring during regeneration
▪ Prognosis poor

70
Q

clinical features of nerve injury

A 
• Sensory features
o Dysaethesiae (disordered sensation)
▪ Anaesthetic
▪ Hypo + hyper aesthetic
▪ Paraesthetic
• Motor
Figure 6 Peripheral Nerve Regeneration
Figure 7 Sunderland Grading of Nerve Injury
o Paresis (weakness)
o Paralysis ± wasting
o Dry skin – loss of tactile adherence since sudomotor nerve fibres not stimulating sweat glands in skin
• Reflexes
o Diminished or absent
71
Q

healing of nerve injuries

A

Healing of nerve injuries is very slow. It starts with initial death of axons distal to the site of injury, Wallerian degeneration and then degradation myelin sheath. Proximal axonal budding occurs after about 4 days. Regeneration proceeds at a rate of about 1mm/day (or 1 inch/month), but in children 3-5mm/day is possible. Pain is the first modality to return. Prognosis for recovery depends on whether the nerve is “pure” (only sensory or motor) or “mixed” and how distal the lesion is (proximal is worse).

72
Q

how can you measure nerve healing?

A

Tinel’s sign can monitor recovery. Tap over the site of nerve and paraesthesia will be felt as far distally as regeneration has progressed. Injury can be assessed, and recovery monitored by electrophysiological nerve conduction studies.

73
Q

describe the rule of 3 for surgical timing in traumatic peripheral nerve injury

A
  1. Immediate surgery within 3 days for clean and sharp injuries
  2. Early surgery within 3 weeks for blunt/contusion injuries
  3. Delayed surgery, performed 3 months after, for closed injuries
74
Q

UMN lesions: strength

A

increased

75
Q

UMN lesions: tone

A

increased

76
Q

UMN lesions: reflexes

A

increased

77
Q

UMN lesions: clonus

A

present

78
Q

UMN lesions: babinski

A

present

79
Q

UMN lesions: atrophy

A

absent

80
Q

LMN lesions: strength

A

decreased

81
Q

LMN lesions: tone

A

decreased

82
Q

LMN lesions: reflexes

A

decreased

83
Q

LMN lesions: clonus

A

absent

84
Q

LMN lesions: babinski

A

absent

85
Q

LMN lesions: atrophy

A

present

Year 3 (164 decks)

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