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MSK Flashcards

1
Q

clincial signs of fractures?

A 
pain 
swelling
crepitus
deformity
adjacent structural injury - vessels, nerves, ligaments, tendons
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2
Q

how to describe a fracture radiograph?

A 
location - epi/dia/metaphysis
fragments 
pattern - transverse, oblique, spiral
displacement?
angulated? valgus(distal away from midline)/varus?
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3
Q

general steps to fracture healing?

A

bleeding
inflammation - neutrophils/macrophages
new tissue - fibro/osteo/chondroblasts
remodelling - macrophages, osteoblasts and clasts

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4
Q

what happens in the inflammation step of fracture healing?

A

haematoma forms
cytokines released
granulation tissue and blood vessel formation

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5
Q

what happens in the repair step of fracture healing?

A

soft callous formation w type II collagen - cartilaginous

hard callous formation w type I collagen - bone

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6
Q

what happens in the remodelling step of fracture healing?

A

callus responds to activity, external forces, functional demands etc (Wolff’s law)
excess bone removed

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7
Q

two types of bone healing?

A

primary : intramembranous ossification - mesenchymal stem cells → osteoblasts (absolute stability)
secondary : endochondral ossification - MSC → chondral precursor → osteoblasts (relative stability) more callous

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8
Q

principles of fracture management?

A

reduce
hold
rehabilitate

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9
Q

reduction options?

A

closed - manipulation / traction

open - mini incision / full exposure

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10
Q

hold options?

A

closed - plaster / traction

fixation - intramedullary pins/nails | extra medullary plate/pins/screws | monoplanar/multiplanar

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11
Q

rehabilitation principles?

A

use - retrain & pain relief
move
strengthen
weight bear

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12
Q

general fracture complications?

A

fat embolus
DVT
infection
prolonged immobility - UTIs, sores

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13
Q

specific fracture complications?

A 
neurovascular/tendon/ligament injury
non/mal union
local infection
degenerative change
reflexive sympathetic dystrophy (excess pain)
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14
Q

what can affect fracture healing?

A 
movement
blood supply
infection
immune function
nutrition
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15
Q

causes of fracture NoF?

A

osteoporosis (old)

trauma (young)

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16
Q

bony landmark division of intra and extra capsular NoF fractures?

A

intratrochanteric line

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17
Q

in which NoF fracture is blood supply more likely to compromised?

A

intracapsular

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18
Q

management for an extracaspualr fracture?

A

fix with plate and dynamic hip screw

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19
Q

management for an intracaspualr fracture? replacement options?

A 
undisplaced = less risk to blood supply → fix with screws
displaced = risk of AVN → replace in older pts(≥55), fix in young

total hip replacement in independent pts
hemiarthroplasty if lower mobility/multiple comorbs

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20
Q

what nerve should be tested in shoulder dislocation?

A

axillary nerve

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21
Q

first line Ix for shoulder dislocation?

A

x ray prior to manipulation

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22
Q

shoulder dislocation management?

A

traction counter traction with gentle internal rotation

adequate pt relaxation - benzodiazepines

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23
Q

what is a hill-sachs defect?

A

deformity of humeral head secondary to shoulder dislocation when it collides with glenoid

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24
Q

management options for distal radius fracture?

A

minimal displacement - cast/splint

instability/child - MUA & K wire

displaced/intraatricular - open reduction internal fixation with plate and screws

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25
Q

management options for tibial plateau fracture?

A

non operative - true undisplaced w good joint line congruancy

operative - restore articular surface using plate and screws , ±bone graft/cement

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26
Q

management options for ankle fracture?

A

non-operative - below knee cast then physio (Weber A/stable B)
operative - ORIF ± syndemsosis repair (Weber unstable B/C)

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27
Q

how can ankle fractures be classified?

A

weber A - below syndesmosis, more stable
weber B - at level of syndesmosis
weber C - fibular fracture above syndesmosis

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28
Q

2 types of low back pain?

A

non-speciifc - no underlying cause found

mechanical - pain after abnormal stress/strain

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29
Q

causes of lower back pain?

A 
mechanical - disc herniation/degenrartion, annular tear, oA
tumours
infection
spondyloarthropy
pars interarticularis injury
visceral
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30
Q

what symptoms indicate sciatica?

A 
unilateral leg pain ≥ back pain 
pain radiating to feet/toes
paraesthesia
straight leg raising test = more pain
localised neurology
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31
Q

when is imaging indicated for back pain?

A

only if it’s likely to change the management (specialist care)

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32
Q

conservative treatment for back pain?

A 
analgesia
NSAIDs
manipulation
acupuncture
massage
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33
Q

red flags for low back pain?

A 
weight loss
fever
 ≤19 yrs
night pain 
= imaging
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34
Q

red flags for leg pain?

A

bowel/bladder dysfunction
saddle anasethisa
neurological deficit
=imaging

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35
Q

what back pain diseases require early diagnosis for effective treatment?

A

myeloma
metastases
inflammatory arthropathy
tuberculosis of spine

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36
Q

imaging for low back pain?

A

MRI - primary

radiographs, CT

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37
Q

different pain therapies?

A 
waiitng
physical therapy
analgesia
facet injections
root blocks
epidural injection - interlaminar, caudal, transforaminal 
neurostimulation
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38
Q

surgical options for back pain?

A

decomprreesison of nerve roots/spinal stenosis
disc replacement
fusion

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39
Q

what is the female athlete triad?

A

disordered etaing
amenhorrhea
osteoporosis
→ stress fractures

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40
Q

how does a stress fracture occur?

A

overuse → stress exerted on bone is greater than its capacity to remodel → bone weakens → stress fracture → ±complete fracture

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41
Q

causes of pathological fractures?

A 
osteoporosis
malognancy
vit d deficiency → osteomalacia/rickets
osteomyeltiis
pages disease
osteogensis imperfecta
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42
Q

causes of secondary osteoporosis?

A

hypogonadism
excess glucocorticoids
alcoholism

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43
Q

pathophysiology of OI?

A

decreased type 1 collagen (abnormal or decreased secretion) → insufficient osteoid production → brittle bones

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44
Q

stages of pages disease?

A

osteoclastic activity
mixed osteoclastic-blastic activity
osteoblastic activity
malignant denegernation

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45
Q

what malignancy is blastic?

A

prostate

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46
Q

what malignancies are lytic?

A

kidney
thyroid
lung

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47
Q

what malignancy is lytic and blastic?

A

breast

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48
Q

primary bone cancers?

A

osteosarcoma
chondrosarcoma
Ewing sarcoma
lymphoma

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49
Q

different types of tendinopathies?

A

tendinosis - abnormal thickening
tendinitis
rupture

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50
Q

how are ligament injuries classified?

A

grade I - slight incomplete tera
grade II - moderate/severe incompleet tear - some joint instability
garde III - complete tearing , obvious instability

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51
Q

treatment options for tendon/ligament tears?

A

immobilise - plaster/boot/brace
or
surgery - suture

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52
Q

disadvantages of immobilisation for injured ligaments?

A

less overall strength of repair
protein degradation ≥ synthesis → ↓ collagen
inferior tissue production by blast cells
resorption of bone at ligament insertion
↓ tissue tensile strength

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53
Q

benefits of mobilisation on injured ligaments?

A

scars are wider stronger and more elastic

better alignment and quality of collagen

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54
Q

outline intramembranous ossification?

A

eg cranial boens and clavicle

mesnchycmal cells condense → differentiate into osteoblasts → ossification centre forms → secreted osteoid traps osteoblasts → osteocytes → trabecular matrix and periosteum form → com[act bones develops → blood vessels condense into red bone marrow

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55
Q

different between primary and secondary ossification centres?

A

primary - site of pre-natal bone growth through endochondral ossifatcion at central part of bone

secondary - post natal bone growth at the physics

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56
Q

outline endochondral primary ossification?

A

mesenchymal differetiaiotn at primary centre → cartilage model of skeleton forms → capillaries penetrate , calcifatcion at primary centre (spongy bone), perichondrium into periosteum → cartilage and chondrocytes continue to grow at ends of bone → secondary centres form

57
Q

outline endochindral secondary ossification?

A

long bone lengthening
happens at physis where theres cartilage
epiphyseal side → hyaline cartilage divides to form HC matrix
diaphysial side → cartilage calcifies and dies → replaced by bone

58
Q

why are children bones more elastic than adults? what can this lead to?

A

↑ density of Haversian canals
plastic deformity - bends before breaking
buckle fractures - column like
greenstick fracture

59
Q

4 differences between child and adult bones?

A

more elastic
physis present
↑ speed of heeling & remodelling

60
Q

when does physis closure complete?

A

girls 15-16

boys 18-19

61
Q

what is developmental dysplasia of the hip?

A

in neonates where head of femur is unstable or incongruous in relation to the acetabulum
dysplasia → sublaxation → dislocation

62
Q

risk factors for developmental dysplasia of the hip?

A 
female
first born
breech
FH
oligohydraminos
swaddling of hip
63
Q

how is developmental dysplasia of the hip usually picked up?

A

baby check

RoM check - limited hip abduction

64
Q

investigations for developmental dysplasia of the hip?

A

US from birth to 4 months

post 4 months - xray

65
Q

treatment options for developmental dysplasia of the hip/

A

reducible hip and <6months : Pavlik harness

failed harness or 6-18months : manipulation under anaesthesia + closed reduction and spica

66
Q

clubfoot alt name?

A

congeniital talipes equinovarus

67
Q

risk factors for clubfoot?

A

hawaiin
M2:1F
genetic PITX1 gene

68
Q

what is the CAVE deformity in clubfoot?

A 
due to muscle contraction
Cavus - high arch, tight FHL, FDL
Adductus of foot  - tight tibialis post and ant 
Varus - tight tendoachilles and TP, TA
Equinous - tight tendoachilles
69
Q

treatment for clubfoot?

A 
ponsetti method is gold standard 
series of casts to correct deformity 
operative treatment 
foot orthosis brace 
± further Sx
70
Q

what is achondroplasia?

A

autosomal dominant in FGFR3

inhibition of chondrocyte proliferation in proliferative zone of physis → defect in endochondral bone formation

71
Q

what is thizomelic dwarfism?

A

humerus shorter than forearm
femur shorter than tibia
normal trunk

72
Q

signs/symptoms of OI?

A 
fragility fractures
short stature
scoliosis
blue sclera
soft brown teeth
worming skull
hypermetabolism
73
Q

what is an avulsion fracture?

A

occurs where ligament/tendon attaches

74
Q

how are phsyeal injuries classified?

A

Salter-Harris classification
1 - physical Separation
2 - fracture transverses physis and exits metaphysis (Above)
3 - fracture transverses physis and exits epiphysis (Lowe)
4 - fracture passes Through epiphysis, physis and metaphysic
5 - crush injury to physis

75
Q

what can physis injuries lead to?

A

growth arrest
whole physis = limb length discrepancy
partial = angulation as unaffected side keeps growing

76
Q

treatment for growth arrest?

A

limb length correction - shorten or lenghtne

angulation - stop growth of unaffected side or reform bone (osteotomy)

77
Q

what’s most often used to restrict fractures in children?

A

splints and plaster

78
Q

first thought for a limping child?

A

septic arthritis - emergency!

79
Q

what can be used to score probability of septic arthritis?

A 
Kocher's classification 
non-weight bearing
ESR ≥ 40
WBC ≥ 12000
Temp ≤36 or ≥ 38
80
Q

what is perthes disease?

A

idiopathic necrosis of the proximal femoral epiphysis
4-8 years old
M4 : 1F

81
Q

4 cause of the limping child?

A

septic arthritis
transient synovitis
perthes disease
SUFE

82
Q

what is transient synovitis?

A

inflamed joint in response to systemic illness

supportive treatment with abx

83
Q

what is SUFE?

A

slipped upper femoral epiphysis - proximal epiphysis slips in relation to metaphysis

84
Q

risk factors of SUFE?

A

obese adolescent males
12 -13 yrs with rapid growth
hypothyroidism/pituitarism

85
Q

treatment for SUFE?

A

screw to prevent further slipping

86
Q

outline the structure of a synocvila joint?

A

synovium - lining containing synoviocytes (A- phagocytic type , B - hyaluronic acid producing) and type I collagen
synovial fluid - hyaluronic acid rich
articular cartilage - type II collagen and preoteoglycan

87
Q

what changes occur during inflammation?

A

↑ blood flow
leukocytes migrate into tissues and are activated/differentiate
cytokines produced - TNFa, IL6,1,17

88
Q

pathogenesis of gout?

A

deposition of uric acid (monosodium urate) crystals in joints → inflammation
rf = hyperuricaemia (genetics, ↑ purine intake,, renal disease)

89
Q

pathogenesis of pseudogout?

A

deposition of calcium pyrophosphate dihydrate → inflammation

rfs = background OA, elderly, intercurrent infections

90
Q

symptoms of gout?

A

gouty arthiritis
tophi - subcutaneous crystals
podagra - MTP joint of big toe affected, ↑ pain, resolves spontaneously

91
Q

how is gout seen on X-rays?

A

rate bite erosions on big toe MTPJ

92
Q

investigations for gout?

A

joint aspiration for synovial fluid analysis

93
Q

gout management?

A

acute - colchicine , nsaids, steroids

chronic - allopurinol

94
Q

how do gout and pseudogout differ in synovial fluid analysis?

A

shape - needle vs brick

birefringence - negative vs positive

95
Q

pathogenesis of RA?

A

abnormal synovial membrane
synovium → proliferated mass of tissue → pannus
due to neovascularisation , lymohangiogenesis , inflammatory cells
cytokine imbalance esp TNFa

96
Q

role of TNFa in RA?

A

dominant pro-inflmamtory cytokine
causes pannus & synovitis
activates osetcolasts → bony erosions
destroys synoviovytes → jt inflammation → pain and swelling
activates chondrocytes → cartilage degradation → jt space narrowing

97
Q

functions of TNFa?

A 
releases proniflmmatory cytokines
hepciidn induction
PGE2 production
chemokine release
endocethelial cell activation → leukocyte accumulation
angiogenesis
chondrocyte activation → ↑ MMP, ↓ cartilage 
osteoclast activation
98
Q

symptoms of RA?

A 
polyarthrits - common in hands and wrists , MCP , PIP< MTP
symmetricla
early morning stiffness 
extensor tenosynovitis
bursitis
99
Q

extra articular manifestations of RA?

A

rheumatoid nodules, fever, weight loss

vasculititis
episcleritis
amyloidosis, lung daisies, felty’s syndrome

100
Q

what can be detected in blood in RA patients?

A

rheumatoid factotr - IgM autoantibody against Fc portion of IgG
antibodies to citrullinated protein antigens

101
Q

what is felty’s syndrome?

A

splenomegaly, leukopenia and RA

102
Q

what are rheumatoid nodules?

A

central area of fibrinoid necrosis surrounded by histiocytes and connective tissue

103
Q

what enzymes mediate citrullination of peptides?

A

peptidyl arginine deaminases

104
Q

management of RA?

A

early recognition of symptoms and aggressive treatment

DMARDs
1st - methotrexate with hydroxychloroquine/sulfasalazine
2nd - biologics, janus kinase inhibitors

prednisolone but not long term
MDT approach

105
Q

biologic options for RA?

A

anti-TNFa - infliximab, etanercept
anti-B cells - rituximab
abatacept
IL-6 inhibitors - tocilizumab

106
Q

what is ankylosing spondylitis?

A 
seronegative spondyloarthropy
chronic sacroilitis
spinal fusion
young males
HLA B27
107
Q

symptoms of ankylosing spondylitis?

A 
lower back pain/stifness in early morning, improves w exercise 
↓ spinal movements
peripheral; arthritis 
achilles tendonitis
fatigue
108
Q

what will blood tests show in ankylosing spondylitis?

A

normocytic anaemia
HLA B27
↑CRP,ESR

109
Q

management for ankylosing spondylitis?

A

phhysio
nsaids
exercise
DMARDs

110
Q

how does psoriatic arthritis present?

A 
assymetrical , IPJs
±symmetrical involvement of small joints
spinal and sacroiliac jt inflammation 
oligoarthritis of large jts
arthritis mutilans - pencil in cup deformity
111
Q

investigations for psoriatic arthritis?

A

xray
MRI - sacroilitis, enthesitis
bloods - seronegative

112
Q

management of psoriatic arhtiritis?

A

DMARDs - methotrexate

113
Q

what is reactive arthritis?

A

sterile inflammation of jts following infetcion , 1-4 weeks (esp urogenital and GI)

114
Q

extra-articular manifestations of reactive arthritis?

A

enthesitis
skin inflammation
eye inflammation

115
Q

what can reactive arthritis often be the first manifestation of?

A

HIV or Hep C

116
Q

what autoantibodies are commonly involved with SLE?

A

antinuclear antibodies - high sensitivity but not specific (quite common in gen pop , needs to be in combo with clinical features)
anti-dsDNA antibodies - high specificity
anti-phospholipid antibodies

117
Q

risk factors for SLE?

A

F9 : 1M
15-40yrs
african/asian ancestry

118
Q

what are the seronegative spondyloarthopathies?

A

ankylosing spondilytis
reactive arthritis
psoriatic arthritis
entreropathic synovitis

119
Q

what is commonly seen in connective tissue disorders?

A

arthralgia and arthritis
autoantibodies
Raynaud’s phenomenon

120
Q

what is reynauds phenomenon?

A

intermittent vasopsams of digits on cold exposure → blanching → cyanosis → rectaove hyperaemia
whites → blue → red

121
Q

clinical manifestations of SLE?

A 
malar rash - spares nasolabial fold
photosensitive rash
mouth ulcers
hair loss
Raynaud's 
arthralgia ± arthritis
serositis
glomerulonephritis
cerebral disease
122
Q

what do anti-phospholipid antibodies increase the risk of?

A

arterial and venous thromboses

123
Q

what will bloods show for SLE?

A 
↑ ESR but normal CRP unless infection, arthritis or serositis
haemolytic anameia, thrombocytopenia
ANAs, anti-dsDNA, antiphospholipid 
low C3 & C4
↓albumin
↑protein:creatine ratio
124
Q

management of SLE?

A

hydroxychloroquine
±maintenance glucocorticoid
methotrexate/azathioprine
biologics

125
Q

what is Sjorgen’s. syndrome?

A

autoimmune exocrinopathy
dry eyes, dry mouth and enlarged parotid gland
non-erosive arthritis and Raynaud’s phenomenon

126
Q

rheumatology diagnostics?

A

bloods
synovial fluid analysis
x rays, US. CT , MRI

127
Q

rheumatology blood tests?

A 
FBC
U&E
LFT
bone profile
ESR
CRP
128
Q

what’s usually raised in FBC of septic arthritis?

A

WCC

129
Q

what can be low in a FBC for inflammatory arthritis?

A

↓Hb

130
Q

why are U&E done in rheumatology?

A

renal impairment eg in SLE, vasculitis, chronic inflammation and with NSAIDs

131
Q

why are LFTs done in rheumatology?

A

DMARDs → liver damage

↓ albumin → ↓ synthesis in liver or leakage form kidneys

132
Q

what will be raised in bone profile for Paget’s disease?

A

↑↑ALP

133
Q

what is synocvial fluid analysis used to diagnose?

A

septic arthritis - gold standard , send for MC&S

crystal arthritis

134
Q

3 differences between septic and reactive arthritis?

A

postive culture, give abx and joint lavage

135
Q

4 X-ray features of OA?

A

loss of joint space
osteophytes
subchondral cysts
subchondral bony sclerosis

136
Q

3 xray features of RA?

A

soft tissue swellling
peri-articular osteopenia
bony erosions

137
Q

US changes in RA?

A

synovial hypertrphy
↑ blood flow
erosions

138
Q

RA vs OA xray?

A

both jt space narrowing
OA : sclerosis and osetophytes
RA : osteopenia, bony erosions

BRS 2 (12 decks)

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