Musculoskeletal Growth/Injury and Repair Flashcards

(85 cards)

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
what factors could alter the first stage in bone healing?
NSAIDs loss of haematoma (open fractures, surgery) extensive tissue damage resulting in poor blood supply
26
what platelet concentrates are implicated in the inflammatory stage of bone healing?
platelet derived growth factor PDGF transforming growth factor beta TGF-b insulin like growth factor IGF vascular endothelial growth factor VEGF
27
stages in bone healing: soft callus
``` 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 ```
28
what can affect the soft callus formation?
replacing cartilage with demineralised bone matrix | placement of bone grafts
29
what would the best autogenous cancellous bone graft have?
osteoconductive osteoinductive best choice
30
what is an allograft bone?
``` cortical cancellous fresh prepared structural osteoconductive not osteoinductive creeping substitution ```
31
what risk is there with bone allografts?
disease transmission
32
stages in bone healing: hard callus
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
33
stages in bone healing: bone remodelling
woven bone converted to lamellar bone medullary canal reconstituted Wolff's law applies
34
what is delayed union?
when a fracture fails to heal in the expected time
35
causes of delayed union
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
in delayed union how could you treat it?
different fixation dynamisation bone grafting
37
what is a tendon?
``` muscle origin from bone muscle belly musculotendinous juntion tendon (? sesamoid bone, ? tendon sheath) tendinous insertion into bone ```
38
structure of tendons
longitudinal arragement of cells (tenocytes) and fibres (type 1 collagen) long narrow spiralling of collagen bundles known as fasicles
39
what are collagen bundles covered by? (Tendons)
endotenon
40
what are tendon fascicles covered by?
paratenon
41
what is a tendon covered with?
epitenon
42
describe a tendon sheath
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
what effect does immobility have on tendons?
reduces water content and glycosaminoglycan concentration and strength
44
what kind of injuries affect tendons?
``` degeneration inflammation enthesiopathy traction apophysitis avulsion +/- bone fragment tear - intrasubstance/musculotendinous junction laceration crush ischaemia attrition nodules ```
45
injuries to tendons: degenration
intrasubstance mucoid degeneration may be swollen, painful, tender, may be asymptomatic ?precursors to rupture
46
what tendon commonly degenerates?
achilles
47
injuries to tendons: inflammation
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
injuries to tendons: enthesiopathy
inflammation at insertion to bone muscle/tendon | usually at muscle origin rather than tendon insertion e.g. lateral humeral epicondylitis (Tennis elbow)
49
give an example of enthesiopathy in a ligament
plantar fasciitis
50
injuries to tendons: traction apophysitis
``` Osgood Schlatter's disease insertion of patellar tendon into anterior tibial tuberosity adolescent active boys recurrent load inflammation ```
51
injuries to tendons: avulsion treatment
conservative - limited application, retraction tendon | operative - reattchment tendon through bone, fixation bone fragment
52
injuries to tendons: intrasubstance rupture
``` 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
injuries to tendons: tear at musculotendinous junction
medial head of gastrocnemius at musculotendinous junction with achilles mis called plantaris syndrome often partial
54
injuries to tendons: laceration
``` E.g. finger flexors (FDS and FDP) ▪ Common ▪ Males > females ▪ Young adults ▪ Repair surgically and early but beware old injuries ▪ Technically challenging ```
55
describe a peripheral nerve
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
function of Aa nerve fibres (IA, IB)
large motor axons muscle stretch tension sensory axons
57
function of Ab nerve fibres (II)
``` touch pressure vibration joint proprioception sensory axons ```
58
function of Ay nerve fibres
efferent motor axons
59
function of Ad nerve fibres (III)
sharp pain very light touch temperature
60
function of B nerve fibres
sympathetic preganglionic motor axons
61
function of C nerve fibres
dull, aching,burning pain | temperature
62
types of injury to nerves
compression | trauma
63
examples of nerve compression injury
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
examples of direct nerve trauma
blow | laceration
65
examples of indirect nerve trauma
avulsion | traction
66
what can nerve trauma result in?
neurpraxia axonotmesis neurotmesis
67
describe neurapraxia
▪ Nerve in continuity ▪ Stretched (8% will damage microcirculation) or bruised ▪ Revisable conduction block – local ischaemia and demyelination ▪ Prognosis good (weeks or months)
68
describe axonotmesis
▪ 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
describe neurotmesis
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
clinical features of nerve injury
``` • 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
healing of nerve injuries
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
how can you measure nerve healing?
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
describe the rule of 3 for surgical timing in traumatic peripheral nerve injury
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
UMN lesions: strength
increased
75
UMN lesions: tone
increased
76
UMN lesions: reflexes
increased
77
UMN lesions: clonus
present
78
UMN lesions: babinski
present
79
UMN lesions: atrophy
absent
80
LMN lesions: strength
decreased
81
LMN lesions: tone
decreased
82
LMN lesions: reflexes
decreased
83
LMN lesions: clonus
absent
84
LMN lesions: babinski
absent
85
LMN lesions: atrophy
present