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BRS 1b > MSK > Flashcards

MSK Flashcards

1
Q

phalanges fracture healing time

A

3 weeks

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2
Q

metacarpals healing time

A

4-6 weeks

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3
Q

distal radius healing time

A

4-6 weeks

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4
Q

forearm healing time

A

8-10 weeks

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5
Q

tibia healing time

A

10 weeks

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6
Q

femur healing time

A

12 weeks

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7
Q

process of indirect fracture healing

A

haematoma formation
cytokine release
granulation tissue and blood vessel formation
soft callus formation (type 2 collagen - cartilage)
converted to hard callus (type 1 collagen - bone)
callus responds to activity, external forces, functional demands and growth
(wolffs law)
excess bone is removed

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8
Q

List some specific and general fracture complications

A

General
- fat embolus
- local infection
- prolonged immobility
- DVT

Specific
- malunion / non union
- degenerative changes
- infection
- reflex sympathies hypertrophy aka complex regional pain syndrome
- neurovascular injury
- muscle / tendon injury

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9
Q

How to prevent embolisms

A

Virchows traid:
Prevent stasis
Prevent coagulation
Fix vessel wall changes

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10
Q

Why do intracapsular NOF fractures heal worse

A

Blood supply is more likely to be compromised, resulting in a vascular necrosis and non union

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11
Q

Which line can you use to help you decide if there has been a hip fracture

A

Shentons line: goes from inside of femoral neck to superior pubic ramus
If unsure if there has been a hip fracture, look to see if she tons line has been disrupted

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12
Q

what should you remember to do in the clinical examination of shoulder dislocation

A

assess neurological status: check if axillary nerve has become damaged

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13
Q

how should you manage a dislocated shoulder

A

tract and counter traction with gentle internal rotation to dis-impact the humeral head
OR
if alone –> Stimson’s method

remember to maintain patient relaxation eg with benzodiazepines

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14
Q

describe a Bankarts and Hill Sachs lesion

A

Bankarts lesion: humeral head moves forwards out of glenoid fossa and by doing so, tears away a price fo the labrum around the glenoid fossa

Hill sachs lesion: back of humeral head impacts with the front of the glenoid fossa, causing a dent in the bone of the head

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15
Q

management of distal radius fracture

A

1) cast/splint:
as a temporary treatment and form of reduction whilst awaiting definitive fixation
or
as a definitive treatment if minimally displaced extra articular fracture

2) MUA (manipulation under anaesthetic) and K wires
for unstable extra articular fractures - esp in children

3) ORIF (open reduction internal fixation)
for displaced unstable fractures that are not suitable for MK wires
or
intra articular fractures

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16
Q

what is lipohaemarthrosis

A

escape of fat and blood from bone marrow into the joint, as the result of an intra articular fracture

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17
Q

what causes a tibial plateau fracture

A

Extreme valgus/varus force or axial loading causes impaction of the femoral condyles with tibial plateau
This causes the comparatively soft bone of tibial plates to depress or split.

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18
Q

management of a tibial plateau fracture

A

non surgical: only of truly undisplaced and has good joint line congruency
surgical: restore articular surface using plates and screws. Use cement in bone graft to prevent further depression after fixation

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19
Q

what is an avulsion fracture

A

An avulsion fracture occurs when a small chunk of bone attached to a tendon or ligament gets pulled away from the main part of the bone

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20
Q

give 4 common causes of mechanical back pain

A

muscular tension
acute muscular sprain or spasm
degenerative disc disease
osteoarthritis of facet joints

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21
Q

describe how a slipped disc causes sciatica

A

the intervertebral disc is made of nucleus pulposus in the middle and annulus fibrosus around the outside.
when the disc slips, the annulus fibrosus tears and the central nucleus pulposus leaks out, impinging the lumbar nerve root

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22
Q

urgent investigation for cauda equina

A

urgent Lumbar MRI spine

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23
Q

causes of cauda equina

A

bony metastases, myeloma, TB, paraspinal abscess, large disc herniation

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24
Q

serious causes of back pain

A

cancer

infection
- staphylococcus, streptococcus, TB, discitis, paraspinal abscess, vertebral osteomyelitis

inflammatory spondyloarthropathy
- ankylosing spondylitis, psoriatic arthritis, IBD related

fracture

referred pain
- kidneys, pancreas, abdominal aneurysm

large disc prolapse

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25
Q

if pt had back pain with a high PSA on blood test, what could the diagnosis be

A

prostate cancer with bony metastases

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26
Q

if pt had back pain and blood test showed high alkaline phosphate, what could the diagnosis be

A

bony metastases

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27
Q

if pt had back pain and blood test showed high calcium, what could diagnosis be

A

myeloma, bony metastases

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28
Q

best imaging for soft tissue structures eg tendons, ligaments

A

MRI

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29
Q

best imaging for spinal cord

A

MRI

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30
Q

treatment for herniated disc

A

NSAIDs
nerve root injection/block
- mixture of analgesia and steroids injected around the swollen or compressed spinal nerve to relieve the pain and inflammation

the disc itself tends to regress back to its original position over time

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31
Q

list the main connective tissue disorders

A

systemic lupus erythematosus
Sjogren’s syndrome
autoimmune musclar inflammatory disease - polymyositis, dermatomyositis
systemic sclerosis (scleroderma) - diffuse or limited cutaneous involvement
overlap syndrome

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32
Q

where do the autoantibodies in rheumatoid arthritis usually attack

A

synovium

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33
Q

what are the autoantibodies in rheumatoid arthritis

A

rheumatoid factor
anti cyclic citrullinated peptide antibody (anti CCP antibody) –> aka ACPA (antibody for citrullinated peptide antigen)

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34
Q

what is ankylosing spondylitis and where is the usual site of inflammation

A

chronic spinal inflammation resulting in spinal fusion and deformity
enthesis
seronegative inflammation

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35
Q

what are the main seronegative spondyloarthropathies

A

ankylosing spondylitis
psoriatic arthiritis
reactive arthritis
enteropathic synovitis

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36
Q

in which group does Lupus usually present

A

females
15-45 yrs old

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37
Q

what is SLE

A

systemic lupus erythematosus - autoimmune inflammation against mostly kidneys, skin, joints

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38
Q

symptoms of SLE

A

malar rash
photosensitive rash
mouth ulcers
alopecia
raynauds
arthralgia and arthiritis
serositis (pericarditis, pleuritis, peritonitis)
cerebral problems
glomerular nephritis

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39
Q

investigations for SLE

A

clinical signs eg malar rash
bloods: anaemia, lymphopenia, thrombocytopenia, high ESR but low CRP
check for presence of autoantibodies - should have high autoantibodies and low complement
thrombosis - due to anti phospholipid AB
proteinuria (urine protein: creatinine ratio)

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40
Q

key points to look for when considering a connective tissue disorder diagnosis

A

arthralgia and arthiritis are non erosive
auto antibodies - may aid with diagnosis and level may correlate with disease severity
raynauds phenomenon (can also be benign)

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41
Q

what is raynauds phenomenon

A

intermittent vasospasms in fingers in cold
1) white –> vasospasm
2) blue –> cyanosis
3) red –> reactive hyperaemia

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42
Q

antibodies in SLE

A

anti nuclear antibody
anti dsDNA antibody
anti phospholipid antibody

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43
Q

antibodies in reactive arthritis

A

none - seronegative

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44
Q

antibodies in systemic vasculitis

A

anti neutrophilic peptide

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45
Q

2 common patterns to look out for with lupus

A

high anti ds DNA antibody with low complement components (C3+4)
high ESR with low CRP

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46
Q

which complement proteins do you test for in lupus

A

C3 and C4

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47
Q

which antibodies do you test for in lupus

A

ANA first - very sensitive but not specific
then dsDNA and anti phospholipid - more specific but less sensitive

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48
Q

most commonly affected joint in gout

A

1st MTP - big toe - podagra

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49
Q

most commonly affected joint in pseudogout

A

knee joint

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50
Q

what is the best test for small joints suspected of gout

A

serum urate
- fine needle aspirate is difficult to do from small joints

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51
Q

what are white opacities in the joint space and what condition do they suggest

A

chonedrocalcinosis –> calcification of cartilage
this finding suggests pseudogout

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52
Q

if an elderly pt is actually unwell with another illness and comes in with painful warm and swollen wrist, what are the most likely diagnoses

A

septic arthritis - infection spread in blood to joint
pseudo gout - commonly affects elderly who are acutely unwell with another illness
reactive arthritis - usually a bit later, 1-4 weeks after the infection

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53
Q

middle aged woman with joint pain in fingers and hands, and swollen finger joints. what are the main differential diagnoses

A

rheumatoid arthritis
lupus - If symmetrical
psoriatic arthritis - more commonly asymmetrical
pseudo gout

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54
Q

investigations if suspect psoriasitoc arthritis

A

check for red scaly skin patch on extensor surfaces
do tests to rule out other causes of join pain
- bloods to check for rheumatoid factor
- fine needle aspiration and synovial fluid analysis to check for gout

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55
Q

best treatment for recurrent psoriatic arthritis

A

DMARDs: methotrexate

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56
Q

what are bridging syndesmophytes and which condition do they suggest

A

ossification of ligaments
- ankylosing spondylitis

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57
Q

what does HLA-B27 positive indicate

A

makes you more susceptible to autoimmune conditions
- reactive arthritis, psoriatic arthritis, ankylosing spondylitis

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58
Q

most commonly affected joints in osteoarthiritis

A

CMC (joint of thumb to hand)
PIP- bouchards
DIP - heberdens

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59
Q

most commonly affected joints in rheumatoid arthiritis

A

MCP
MTP
PIP
wrists, knees, ankles

60
Q

What are the components of a synovial joint and describe each of them?

A

Synovium - 1-3 cell deep lining containing macrophage-like phagocytic cells (type A synoviocyte) and fibroblast-like cells that produce hyaluronic acid (type B synoviocyte). Type I collage also present.

Synovial fluid - Hyaluronic acid-rich viscous fluid.

Articular cartilage - Type II collagen + Proteoglycan (aggrecan)

61
Q

what are the primary inflammation and secondary inflammation causes of arthiritis

A

primary inflammation
- autoiumme (lupus, psoriatic, reactive, rheumatoid)
secondary inflammation
- infection (TB, septic)
- crystal arthritis (gout, pseudogout)

62
Q

what are the sterile and non sterile inflammatory causes of arthiritis

A

sterile
- autoimmune
- crystal arthiritis
non sterile
- infectious

63
Q

why are children bones more elastic

A

increased density of Haversian canals

64
Q

increased elasticity of children’s bones lead to which 3 types of bone deformities

A

plastic deformity (bone bends)
torus/buckle fracture
greenstick fracture

65
Q

name of fracture where piece of bone is pulled off by ligament/tendon

A

avulsion fracture

66
Q

describe intramembranous ossification

A
  • condensation of mesenchymal cells which differentiate into osteoblasts
  • leads to formation of ossification centre
  • osteoid is secreted which traps oestoblasts, causing them to convert into osteocytes
  • trabecular matrix and periosteum formation
  • compact bone develops superficial to the cancellous bone
  • crowded blood vessels condense to form red bone marrow
67
Q

where does intramembranous ossification happen

A

cranial bones, clavicle, mandible

68
Q

what are primary ossification centres

A

sites of prenatal bone growth - endochondral ossification
in central part of bone

69
Q

where does endochondral ossification happen

A

all long bones at primary and secondary ossification centres

70
Q

what are secondary ossification centres

A

sites of post natal bone growth
in physis, long bones have several of them

71
Q

in which type of fractures does direct fracture healing often occur

A

intra-articular fractures - so doesn’t cause post traumatic arthiritis

72
Q

what scan is done to see a paediatric joint below the age of secondary ossification

A

arthrogram - allows you to see cartilage

73
Q

describe briefly how long bones are lengthened

A

at the physis: endochondral secondary ossification (endochonral bone growth at secondary ossification centres)
epiphyseal side: hyaline cartilage is active and dividing to form hyaline matrix
diaphyseal side: cartilage calcifies and dies and is replaced by bone

74
Q

main differences in structure of bones in children vs adults

A

children:
- have physis
- more elastic
- thicker periosteum
- immature bone - less dense + greater porosity
- greater speed of healing

75
Q

what are the two different types of growth arrest

A

whole physis –> limb length discrepancy
partial –> angular deformity

76
Q

how to fix limb length discrepancy vs angular deformity

A

limb length discrepancy: shorten unaffected bone or lengthen affected bone

angular deformity: stop growth in the unaffected side of the bone or reform the bone (osteotomy)

77
Q

what are the main forms of external and internal restriction

A

external: splinter, plaster
internal: plates + screws, intra medullary device

78
Q

what is developmental dysplasia of the hip and in which group is it most common

A

femoral head not congruent with acetabulum
can be sublaxation (they still touch but not congruent) or dislocation (don’t even touch)
most common in
- females
- first born
- breech
- family history
- oligohydramnios

79
Q

investigations for developmental dysplasia of the hip, and what is the most indicative clinical sign

A

check range of motion: most indicative clinical sign = limited abduction
check limb length discrepancy: Galeazzi’s sign
for <3 months: can do Barlow and Ortalani manoeuvre (checks if femoral head can be dislocated out of acetabulum (Barlow) and then pushed back in (ortolani))

after this need to do imaging
<4 months = USS
>4 months = x ray

80
Q

treatments for developmental dysplasia of the hip

A

for reducible hip and <6months
- palvik harness

if palvik harness doesn’t work/ >6months:
- MAU (closed reduction)
- spica

81
Q

what is congenital talipes equinovarus and what are the main features

A

club foot
CAVE
Cavus - high arch of foot
Adductus - front of foot/toes pointed medially
Varus - whole foot twisted from outside inwards
Equinous - limited flexibility of ankle and ability to dorsiflex

82
Q

which group is congenital talipes equinovarus most common in

A

males and Hawaiian

83
Q

treatment for congenital talipes equinovarus

A

ponseti method (series of casts)
may need surgery
Foot orthosis brace

84
Q

genetic cause of congenital talipes equinovarus

A

PITX1 Gene

85
Q

what is the genetic hereditary pattern of achondroplasia

A

autosomal dominant

86
Q

genetic cause of achondroplasia

A

G380 mutation in FGFR3 gene

87
Q

what is achondroplasia

A

inhibited chondrocyte proliferation in the proliferative zone of the physis
results in defects of endochondral bone growth

causes Rhizomelic dwarfism

88
Q

describe the dwarfism of achondroplasia

A

rhizomelic dwarfism
- humerus shorter than forearm
- femur shorter than tibia
- trunk size normal

89
Q

what is the genetic hereditary pattern of osteogenesis imperfecta

A

autosomal dominant or recessive

90
Q

cause of osteogenesis imperfecta

A

decreased type 1 collagen (cartilage) due to either
- reduced secretion
or
- abnormal production

–> lead to decreased osteoid secretion

91
Q

orthopaedic manifestations of osteogenesis imperfecta

A

brittle bones (fragility fractures)
scoliosis
short stature

92
Q

non orthopaedic manifestations of osteogenesis imperfecta

A

heart issues
blue sclera
dentinogenesis imperfecta (soft brown teeth)
wormian skull
hyper metabolism

93
Q

what is kochers classification for septic arthritis

A

non weight bearing
temp > 38
WBC >12 000
ESR > 40

94
Q

what is it more likely to be if it doesn’t fulfil kochers classification

A

transient synovitis

95
Q

main 3 dangerous causes of limping child, and which should you rule out first

A

septic arthritis (1st!!)
perthes disease
SUFE

96
Q

what is perthes disease, which group is it most common in and how do you treat

A

idiopathic necrosis of proximal femoral epiphysis
males, 4-8yrs old
supportive therapy, will grow back

97
Q

what is SUFE, which group is it most common in and how do you treat

A

Slipped upper femoral epiphysis (proximal epiphysis slips in relation to metaphysis)
obese adolescent males
operative fixation using screw

98
Q

what are osteocytes

A

mature bone cells embedded in matrix
formed when osteoblasts get trapped in their secretions and mature

99
Q

where are osteogenic cells found

A

deep layers of periosteum

100
Q

what is in the medullary cartilage

A

nutrient artery

101
Q

what are volkmans canals

A

transverse canals which allow communication of periosteum with bone and between Haversian canals

102
Q

structure of osteon

A

central Haversian canal (vein, artery, nerve, lymphatic)
surrounded by concentric lamellae
lacunae seen between lamellae - contain osteocytes
canaliculi radiate from lacunae and connect them with each other
volkmans canals - transverse - connect haversions canals

103
Q

3 types of fracture

A

trauma - high/low energy
stress
pathological

104
Q

4 scans for fracture

A

radiograph
MRI
CT
bone scan

105
Q

management for extracaspular NoF fracture

A

internal fixation

106
Q

management for undisplaced intracaspular NoF fracture

A

fixation with screws

107
Q

management for displaced intracaspular NoF fracture

A

if <50: reduce and fixate with screws
if >50 and fit: full hip replacement
if >50 and unfit: hemiarthoplasty

108
Q

what is cartilage made of

A

Specialised cells → Chondrocytes

ECM: Water, collagen and proteoglycans (mainly aggrecan)

109
Q

what is aggrecan and what is it characterised by

A

Proteoglycan possessing many chondroitan sulphate and keratin sulphate chains

Characterised by ability to interact with hyaluronan (HA) to form large proteoglycan aggregates

110
Q

what are the main radiographic features seen in OA

A

LOSS
Loss of joint space
Osteophytes
Sclerosis
Subchondral cysts

111
Q

what is infection of the bone called and how is out treated

A

osteomyelitis
surgical drainage and IV antibiotics
in severe cases - amputation

112
Q

conservative OA management

A

physiotherapy
walking aid
analgesia
steroid injection

113
Q

what is joint impingement

A

painful condition caused by friction of joint tissues

114
Q

list some red flags for back pain

A

worse in morning/when supine
thoracic pain
bladder or bowel disturbances
altered sensation
fever
weight loss
night sweats
pain is getting progressively worse
older age or younger age
previous malignancy
currently immunosuppressed

115
Q

which blood tests do you do for back pain

A

ESR - myeloma, chronic inflammation, TB
CRP - infection, inflammation
FBC - check for anaemia (myeloma, chronic inflammation) or raised WCC (infection
ALK (alkaline phosphate) - bony mets, myeloma
PSA - prostate cancer mets

116
Q

3 main types of inflammatory spondyloarthiritis

A

ankylosing spondylitis
psoriatic arthiritis
IBD

117
Q

4 main extra articular manifestations of inflammatory SpA

A

4 A’s:
anterior uveitis
aortitis /aortic regurgitation
apical lung fibrosis
amyloidosis

118
Q

what happens if you leave ankylosing spondylitis untreated

A

spinal enthesitis –> bridging syndesmophytes –> spinal fusion

119
Q

main articular features of akylsoing spondylitis

A

spondylitis
sacroilitis
ethesitis

120
Q

treatment for ankylosing spondylitis

A

pshyiotherapy
1st line: NSAIDs
2nd line: Biologics

121
Q

what can you take with NSAIDs to reduce risk of GI ulcer

A

selective COX2 inhibitors eg celecoxib

122
Q

important cytokines in ankylosing spondylitis

A

IL17
IL23
TNF alpha

123
Q

important genetic component in ankylosing spondylitis

A

HLA-B27

124
Q

describe Types A,B,C of webers classification

A

A: fibula is fractured below the tibial plafond: syndesmosis not affected
B: fibula is fractured at level of the tibial plafond: syndesmosis affected in 50% off cases
C: fibula is fractured above the tibial plafond: syndesmosis always affected

125
Q

What causes septic arthritis?

A

Bacterial infection of a joint (usually caused by haematogenous spread)

126
Q

septic arthritis risk factors

A

Immunosuppressed, pre-existing joint damage, intravenous drug use (IVDU)

127
Q

What bacteria are commonly responsible for septic arthritis?

A

Staphylococcus aureus, Streptococci, Gonococcus

128
Q

How many joints are usually affected in septic arthritis? And what is the main exception?

A

1 (mono-arthritis)
Gonococcal septic arthritis - often affects multiple joints (polyarthritis); it is less likely to cause joint destruction.

129
Q

septic arthritis treatment

A

surgical lavage and IV antibiotics

130
Q

what is gout caused by and what is a risk factor for gout?

A

uric acid crystals deposited in joints causing inflammation
Hyperuricaemia: High uric acid levels in blood → Risk factor for gout (not everyone who has high levels will have develop attacks of gout)

131
Q

What are the causes of hyperuricaemia?

A

Genetic tendency
Increased uptake of purine rich foods (Purine gets broken down into uric acid → Beer drinkers particularly vulnerable).
Reduced excretion (kidney failure) of uric acid

132
Q

what is pseudo gout caused by and what are the risk factors

A

Syndrome caused by deposition of calcium pyrophosphate dihydrate (CPPD) crystals → Crystals lead to inflammation.
Background osteoarthritis, elderly patients, intercurrent infection.

133
Q

clinical features of gout and most commonly affected joints

A

Typically presents with anacute mono-arthritis. First MTP joint is the most commonly affected joint (Podagra = gout of the foot, esp the big toe)

Other joints affected → joints in foot, ankle, knee, wrist, finger and elbow are most frequently affected.

Crystal deposits (tophi)developing around hands, feet, elbows and ears. → Yellowish appearance

134
Q

The diagnosis of crystal arthritis is made by aspirating fluid from affected joint and examining under a microscope using polarised light.What would you see for gout and pseudo-gout?

A

Gout - needle-shaped crystals with -ve birefringence.

Pseudo-gout - rhomboid shaped crystals with +ve birefringence.

(Birefringence is the optical property of a material having a refractive index that depends on the polarization and propagation direction of light)

- p for pseudo gout, p for positive
- rhomboid is tilted so its the one that is refracted
135
Q

The primary site of pathology for rheumatoid arthritis is in the synovium (inflammation occurs here). What 3 things does this include?

A

Synovial joints
Tenosynovium surrounding tendons
Bursa (fluid-filled sacs that provide lubrication to allow easy movement)

136
Q

The presence of which extra articular feature confirms diagnosis of RA?

A

subcutaneous/rheumatoid nodule: is invariably associated with the rheumatoid factor

137
Q

What is the pattern of joint involvement in rheumatoid arthritis?

A

Symmetrical
Affects small and large joints, but particularly hands and feet.
Commonest affected joints:
MCP
MTP
PIP
Wrists
Knees

138
Q

What is Felty’s syndrome?

A

triad of splenomegaly (enlarged spleen), leukopenia (low WBC count) and RA

139
Q

What are the common and uncommon extra-articular features of rheumatoid arthritis?

A

Common

Fever, weight loss

Subcutaneous nodules

Uncommon

Vasculitis

Ocular inflammation - episcleritis

Neuropathies (damage to nerves) 

Amyloidosis (**a group of rare, serious conditions caused by a build-up of an abnormal protein called amyloid in organs and tissues throughout the body**. The build-up of amyloid proteins (deposits) can make it difficult for the organs and tissues to work properly)

Lung disease - nodules, fibrosis, pleuritis (inflammation of pleura which are the lining of the lungs)

Felty's Syndrome - triad of splenomegaly, leukopenia and RA
140
Q

causes (genetic and environmental) of RA

A

HLA- DR
other genes: PTPN22, IL6R

environmental:
smoking
microbiome
porphyromonas gingivalis
poor oral health

141
Q

describe the composition of the subcutaneous nodules in RA

A

centre of fibroid necrosis
surrounded by histiocytes + connective tissue

142
Q

describe the formation of a pannus in RA

A

Neovascularisation
Lymphangiogenesis
Inflammatory cells → activated B and T cells, plasma cells, mast cells and activated macrophages.

There is an excess of pro-inflammatory (IL1, TNF alpha) vs. anti-inflammatory (soluble tNF receptor, IL10, TNF receptor agonist) cytokines

143
Q

whta is the main inflammatory cytokine in RA and describe how it affects the joint/causes the diseases

A

stimulates
- chondrocytes: cartilage degradation –>joint space narrowing
- osteoclasts: bone erosion
- synoviocytes: joint inflammation and pain

144
Q

describe how researchers found TNF alpha to be the main inflammatory cytokine in RA

A

they inhibited it using monoclonal antibodies (inflixumab and adalimumab) and soluble TNF receptor fusion proteins (etanercept)
as a results the other inflammatory cytokines IL 1,6,8, GMCSF were blocked

145
Q

what is rheumatoid factor

A

IgM anti IgG antibody

146
Q

what are anti cyclic citrullinated peptide antibodies and which reaction do they target

A

arginine – (PADs: peptide arginine deiminases) –> citrulline

BRS 1b (10 decks)

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