MSK Flashcards
2 major divisions of arthritis
OA (degenerative)
inflammation
3 main causes of joint inflammation
- infection
- crystal arthritis
- immune mediated (autoimmune)
which one is primary joint inflammation
autoimmune
which one is secondary joint inflammation
infection and crystal arthritis
examples of infection in joint inflammation (2)
septic arthritis
TB
examples of crystals arthritis in joint inflammation (2)
gout
pseudogout
which are sterile joint inflammation
crystal arthritis
autommune
which are non sterile joint inflammation
septic arthritis
TB
speed of onset of OA
slow
speed of onset of immune mediated arthritis
subacute
speed of onset of crystal arthritis and septic arthritis
rapid
which arthritis has both CRP & WCC elevated
septic arthritis
what is the key investigation of septic arthritis
joint aspiration and send fluid for gram stain and culture
management of septic arthritis
lavage (joint washout) and IV antibiotics
what are the 3 kinds of autoimmune arthritis
- lupus
- seronegative arthritis
- rheumatoid arthritis
where is the primary site of pathology of RA
synovium
where can synovium be found
synovial joints
tenosynovium surrounding tendons
bursa
sex bias of RA
F:M = 2:1
features of RA (4)
polyarthritis
chronic
pain, swelling, morning stiffness
joint erosions
what are detected in blood in RA
autoantibodies
what is the strongest genetic risk factor in RA
HLA-DR
what are in HLA class 1
HLA class A, B , C
what are in HLA class 2
HLA class D
where are HLA class 1 expressed on
all cells
what are associated with HLA class 1
CD8 killer cells
where are HLA class 2 expressed on
only on APCs eg dendritic cells, macrophages, B cells
what are associated with HLA class 2
CD4 helper cells with B cells
HLA class 1 associate with which disease in RA
ankylosing spondylitis
which HLA associate with ankylosing spondylitis
HLA-B27
why autoantibodies in RA but no ankylosing spondylitis
HLA class 2 implicates CD4 T cells and B cells
RA pattern of joint involvement (symmetry or not, how many joints, large or small joint)
symmetrical
polyarthritis
always small joints invovled
where do RA most commonly affect
hand and feet
common affected joints by RA
MCPJ
PIPJ
wrists
knees
ankles
MTPJ
which arthritis associate with morning stiffness
RA
which arthritis associate with worse with activities
OA
which joints are affected by OA
DIPJ
PIPJ
thumb CMCJ
MCPJ
what are some systemic symptoms of RA
fatigue
fever
weight loss
what are some organ-specific extra-articular features of RA
subcutaneous nodules
lung diseases (ILD, fibrosis, pleuritis)
vasculitis
neuropathies
amyloidosis
ocular inflammation (eye episcleritis)
felty’s syndrome
where are subcutaneous nodules found in RA
central area of fibrinoid necrosis surrounded by histiocytes and peripheral layer of connective tissues
what can be found in RA in blood
rheumatoid factors (Ab that bind to IgG)
anti CCP antibodies
what is pannus in RA
synovium becomes proliferated mass of tissue due to neovascularisation, lymphangiogenesis, inflammatory cells
what cells does healthy synovial membrane has
macrophage like (type A synoviocyte)
fibroblast like (type B synoviocyte)
type 1 collagen
what are different types of RA pathogenesis (cellular and molecular pathways)
autoreactive B cells
autoreactive T cells
cytokines (TNF alpha, IL-6, IL-1)
treatment for autoreactive B cells RA
rituximab
treatment for autoreactive T cells RA
abatacept
treatment for cytokine related RA
anti-TNF alpha, anti IL-6 receptor
which cytokine is dominant pro-inflammatory cytokine in rheumatoid synovium
TNF-alpha
pathogenesis of TNF-alpha RA
inflammtory cell recruitment, angiogenesis, lymphangiogenesis, –> pannus formation
matrix matalloproteases –> cartilage loss
osteoclast activation –> bone loss (osteopenia, erosions)
blood test findings in RA
increase ESR, CRP
autoantibodies
what does ACPA do in RA
causes chronic joint destruction and systemic inflammation
Xray features in RA (3)
soft tissue swelling
peri-articular oeteopenia
bony erosions
which is better scan for RA
USS
USS features of RA
synovial thickening (synovial hypertrophy)
increased blood flow (doppler signal)
can detect erosion not found on RA
why not MRI for RA
expensive
time consuming
why need aggressive pharmacological treatment for RA
suppress inflammation
pharmacological treatment for RA
glococorticoid (steroids)
DMARDs(disease modifying anti-rheumatic drug)
first line pharmacological treatment for RA
combine DMARD therapy (methotrexate+hydroxychloroquine +/or sulfasalazine) and IM or oral steroid short course
second line pharmacological treatment for RA
biological therapies eg anti-TNF alpha blockade
methods to administer steroid in RA (4)
oral prednisolone
IM methyl prednisolone
IV
Intra - articular (IA)
steroid side effects
cushing’s syndrome
what is the scoring system for RA
DAS28 score
components of DAS28 scoring in RA
number of tender joints
number of swollen joints
patient visual analogue score (VAS)
ESR/ CRP
what are some biological therapies targeting cytokines in RA
inhibit TNF-alpha and IL-6
antibodies to inhibit TNF-alpha
infliximab
adalimumab
golimumab
cetrolizumab
antibodies to inhibit IL-6 receptor
tocilizumab
sarilumab
biological therapies targeting lymphocytes
B cell depletion
block T cell co-stimulating
example of biological therapies to target B cell depletion
Rituximab (IV infusion)
example of biological therapies to target blocking T cell co-stimulation
adatacept
what is seronegative inflammatory arthritis
RF CCP antibodies not present in blood
but are immune mediated
examples of seronegative inflammatory arthritis (3)
psoriatic arthritis
reactive arthritis
ankylosing spondylitis
what is psoriatic arthritis
immune mediated disease affecting skin
where does psoriatic arthritis mainly affect
skin
extensor surfaces (elbow, knees)
some also has joint inflammation
dominant pathogenic pathway in psoriatic arthritis
IL17-IL23
what are some clinical signs of psoriatic arthritis
nail pitting
onycholysis (nail separate from nail bed)
which joints do psoriatic arthritis affect
IPJs
tendon insertions (enthesitis), can hv sausage finger
is psoriatic arthritis symmetrical
can be both
asymmetric in IPJ
symmetric in small joints
what are some manifestations of psoriatic arthritis
spinal and sacroiliac joint inflammation
oligoarthritis of alrge koints
arthritis mutilans
symmentric involvement of small joints
what is reactive inflammation
sterile inflammation followed by infection elsewhere in body
what are some common infections causing reactive
urogenital infections
gastrointestinal infection (eg salmonella)
extra-articular manifestations in reactive arthritis
enthesitis (tendon inflammation)
skin inflammation
eye inflammation
reactive arthritis can be first manifestation of which disease
HIV
Hepatitis C infection
is septic arthritis same as reactive arthritis
no
difference between septic arthritis and reactive arthritis in terms of synovial fluid culture
septic: positive
reactive: sterile
difference between septic arthritis and reactive arthritis in terms of antibiotic therapy
septic: yes, IV
reactive: no (but yes for treating underlying infection of STI)
difference between septic arthritis and reactive arthritis in terms of joint lavage
septic: yes
reactive: no
In trauma, what are the 3 main components in hold
plaster
external fixator
internal fixator
how long is rehab in truama
~6 weeks
ABCD in truama
airway
breathing
circulation
disability
what to look for when assessing fractures
pain
swelling
crepitus
deformity
collateral (nerve, vessel)
imaging for investigations in fractures
XRay
CT
MRI
what is CT for in assessing fractures (2)
assess pattern and make diagnosis
how to describe a fracture radiograph (6)
Location: which bone and which part of bone?
Pieces: simple/multifragmentary?
Pattern: transverse/oblique/spiral
Displaced/undisplaced?
Translated/angulated?
X/Y/Z plane
what are the 4 types of displacement in trauma fractures
translation
angulation
rotation
impaction
what kind of translation of displacement in trauma fracture (4)
medial
lateral
dorsal
volar
what kind of angulation of displacement in trauma fracture (2)
valgus
varus
when is direct fracture healing possible? (3)
1.anatomical reduction
2. absolute stability / compression
3. no callus or deformity
when is indirect fracture healing possible? (3)
- Sufficient reduction
- Micromovement
- Callus
3 stages of indirect fracture healing
- inflammation
- repair
- remodelling
what is wolff’s law in indirect fracture healing
Bone Grows and Remodels in response to the forces that are placed on it
steps in indirect fracture healing (4)
- haematoma formation
- fibrocartiliginous callus formation
- bony callus formation
- bone remodelling
what is involved in inflammation stage in indirect fracture healing (3)
- Haematoma formation
- Release of Cytokines
- Granulation tissue and blood vessel formation
what is involved in repair stage in indirect fracture healing (2)
- Soft Callus formation
(Type II Collagen - Cartilage) - Converted to hard callus
(Type I Collagen - Bone)
what is involved in remodelling stage in indirect fracture healing (2)
- Callus responds to activity, external forces, functional demands and growth
- Excess bone is removed
2 kinds of reduction in management of fractures
closed
open
3 kinds of hold in management of fractures
Plaster/splint
External fixation
Internal fixation
3 kinds of rehabiliate in management of fractures
Early / late
Weight bearing
Physiotherapy
2 kinds of closed reduction in management of fractures
manipulation
traction
2 kinds of open reduction in management of fractures
mini incision
full exposure
how to describe fixations (3)
internal/external
intra/extra medullary
mono/multiplanar
general fracture complication examples
Fat embolus
DVT
Infection
Prolonged immobility (UTI, chest infections, sores)
specific fracture complication examples
Neurovascular injury
Muscle/tendon injury
Non union/mal union
Local infection
Degenerative change (intraarticular)
Reflex sympathetic dystrophy
what are mechanical factors affecting healing (2)
movement
forces
what are biological environment factors affecting healing (4)
blood supply
immune function
infection
nutrition
causes of fractured of neck of femur (3)
Osteoporosis (older)
Trauma (younger)
Combination
what’s important in history for fractured neck of femur
Age
Comorbidityrespiratory/cardiovascular/diabetes/cancer
Preinjury mobilityindependent/shopping/walking/sports
Social hx: relatives, stairs, alcohol
what are different types of neck of femur fractures
subcapital
transcervical
basicervical
subtrochanteric & intertrochanteric (both not femur fractures technically)
which of the femur fractures is intracapsular
subcapital
which of the femur fractures is extracapsular
transcervical
basicervical
what are the 2 types of problems arouse from neck of femur fracture for blood supply compromised
avascular necrosis
non-union(broken bone fails to heal)
exeample of management of neck of femur fractures for extracapuslar fractures
DHS (dynamic hip screw)
presentation of shoulder dislocation
pain
restricted movement
loss of normal shoulder contour
related to direct trauma usually
which neurovascular status need to be assessed in shoulder dislocation
axillary nerve
investigation for shoulder dislocation
x-ray to identify fracture (humeral neck, glenoid etc)
what is the safest management for shoulder dislocation
traction countertraction +/- gentle internal rotation to disimpact humeral head
management of shoulder dislocation
adequate analgesia , vigorous/twisted manipulation should be avoided to avoid fractures
traction
what are the 3 views for xray in shoulder dislocation
AP
true AP
Y-view
what is hill-sachs defect in shoulder dislocation
defect at humerus head under glenoid
temporary management of any distal radius fracture
reduction of fracture and placement into cast until definitive fixation
exrtra-articular secpfic distal radiu fracture management
MUA and K-wire fixation
distal radius fracture not suitable for K-wires or intra-articular fracture management
Open Reduction Internal Fixation (ORIF) with plate and screws
main function of proximal tibial
key weightbearing surface of knee joint
what can cause tibial plateau fracture
valgus or varus force
axial loading across knee
impaction pf femoral condyles cause soft bone of tibial plateau
non-operative management of tibial plateau fracture
CT imaging
operative management of tibial plateau fracture
restore articular surface using combination of plate and screws
bone graft or cement to prevent further depression after fixation
non operative management of ankle fracture
non-weightbearing below knee cast for 6-8 weeks, can transfer to walking boot then PT
what is weber A fracture
below syndesmosis and thought to be stable
what is weber B fracture
fracture at same level of syndesmosis
do weber A or B need operative management
no
weber B if no instability then no need
operative management for ankle fracture
Open reduction internal fixation (ORIF)
what is weber C fracture
above level of syndesmosis therefore unstable
curvature of cervical and lumbar in spine
normal lordosis
curvature of thoracic spine
kyphosis
how many bones do vertebrae of spine have
24 (7C, 12 T, 5L)
function of intervertebral discs (2)
shock absorber
allow segmentation and multi-directional movement
what does the spinal column made up of (4)
vertebrae
muscles
intervertebral joints
facet joints
which level does spinal cord end
L2 vertebrae
where do we do lumbar puncture
L3-4
what is the most distal part of spinal cord called
conus medullaris
what are the movements of the spine (4)
flexion
extension
lateral flexion
rotation
what is important to distinguish in terms of back pain (2)
mechanical back pain and serious pathology
which type of back pain is usually self limiting
acute back pain
characteristic of mechanical back pain (2)
reproduced
worse with movement
common causes of mechanical back pain (4)
-Muscular tension (e.g. chronic poor posture, weak muscles)
-Acute muscle sprain/spasm
-Degenerative disc disease
-Osteoarthritis of facet joints
what is sciatica
pain radiating down one leg
causes of sciatica
disc herniation contacting the exiting lumbar nerve root
causes of back pain (7)
tumor
infection
inflammatory spondyloarthropathy
fracture
large disc prolapse
referred pain (pancreas, kidney, aortic aneurysm)
bacteria that cause back pain
Staphylococcus, streptococcus, tuberculosis (TB)
infection causes of back pain (4)
Discitis
Vertebral osteomyelitis
Paraspinal abcess
Microbiology: Staphylococcus, streptococcus, tuberculosis (TB)
inflammatory causes of back pain
ankylosing spondylitis, psoriatic arthritis, inflammatory bowel disease (IBD)-associated
what are the red flags of back pain
Pain at night or increased pain when supine
Constant or progressive pain
Thoracic pain
Weight loss
Previous malignancy
Fever/night sweats
Immunosuppressed
Bladder or bowel disturbance (Sphincter dysfunction)
Leg weakness or sensory loss
Age <20 or >55 yrs
symptoms or signs of cauda equina syndrome
Saddle anaesthesia (loss of sensation)
Bladder/bowel incontinence
Loss of anal tone on PR
Radicular leg pain
Ankle jerks may be absent
investigation of cauda equina syndrome
MRI L spine
causes of cauda equina syndrome
large disc herniation, bony mets, myeloma, TB, paraspinal abcess
treatment for cauda equina syndrome
surgery
do we need investigations in absence of red flags
no
what are the treatment for low back pain without red flags
analgesia (NSAIDS, ibuprofen, paracetamol, codeine)
avoid bed rest
Physiotherapy
blood tests components to test for back pain
ESR
CRP
FBC
ALP
calcium
PSA
increase ESR indications in back pain
increase in myeloma
chronic inflammation
TB
increase alkaline phosphatase(ALP) indication
bony metastases
imaging investigations for back pain
X-ray
CT
MRI
advantages and disadvantages of using MRI for back pain
-Best visualization of soft tissue structures like tendons and ligaments
-Best for spinal imaging: can see spinal cord and exiting nerve roots
-Expensive and time-consuming
treatment for herniated disc
- Conservative as for LBP without sciatica
-Analgesia especially NSAIDs
-Physiotherapy to improve core strength and treat associated muscle spasm - Nerve root injection (local anaesthetic and glucocorticoid)
- Surgery if neurological compromise or symptoms persist
examples of inflammatory spondyloarthritis (SpA)
ankylosing spondylitis
psoriatic arthritis
IBD
where are the most common inflammation site of Spondyloarthritis
spine (spondylitis) and sacro-iliac joints (sacro-iliitis), peripheral joints, entheses (tendon insertions)
what are some extra-articular manifestations of inflammatory spondyloarthritis (4As)
Anterior uveitis (iritis) – ocular inflammation
Apical lung fibrosis
Aortitis/aortic regurgitation
Amyloidosis – due to chronically serum amyloid A (SAA) depositing in organs
major characteristic of ankylosing spondylitis
enthesitis
loss of spinal movement
strongest genetic risk factor of ankylosing spondylitis
HLA-B27
is ankylosing spondylitis mono or poly genetic
polygenetic
what are the cytokines that are important in ankylosing spondylitis (3)
- tumour necrosis factor alpha (TNF-alpha)
- interleukin-17 (IL-17)
- interleukin-23 (IL23)
what features on MRI of sacroiliac joint suggest inflammation of bone marrow
white on either side of sacroiliac joint
features of untreated ankylosing spondylitis
Spinal enthesitis
Bridging syndesmophytes
(new bone growth between adjacent vertebra)
Spinal fusion
what feature on MRI suggest ankylosing spondylitis
shiny corners
management of ankylosing spondylitis
- physiotherapy
- Medicine (NSAIDs, biological therapies)
examples of pharmacological treatment for ankylosing spondylitis
1st line: NSAIDs
-e.g. ibuprofen,
-Selective COX2 inhibitors (e.g. celecoxib) reduce GI ulcer risk
2nd line: ‘Biological’ therapies
Therapeutic monoclonal antibodies (mAbs) targeting specific molecules
Use if inadequate disease control after trying 2 NSAIDs
Anti-TNF-alpha (e.g. infliximab, golimumab)
Anti-IL17 (e.g. secukinumab)
what are overlap symptoms in autoimmune connective tissue disorders
have both lupus and inflammatory
examples of autoimmune connective tissue disorders
SLE
scleroderma
autoimmune inflammatory muscle disease
sjogren’s syndrome
where is main site of inflammation in RA
synovium
what are the autoantibodies associated with RA (2)
Rheumatoid factor
anti CCP(citrullinated peptide) antibodies
does ankylosing spondylitis have autoantibodies
no, it is seronegative
examples of seronegative inflammatory arthritis
Ankylosing spondylitis
Reactive Arthritis
Arthritis associated with psoriasis (psoriatic arthritis)
Arthritis associated with gastrointestinal inflammation (enteropathic arthritis)
where is site of inflammation in ankylosing spondylitis
spinal inflammation
enthesis (tendon, ligament, joint capsule)
does SLE affect innate or adaptive immune system
both
where are site of inflammation of SLE
multi-site
joints
skin
kidney
what is raynaud’s phenomenon
color change in hand and feet
what is typical color change in raynaud’s phenomenon and what do colors mean (3)
WHITE -> Vasospasm leads to blanching of digit
BLUE -> Cyanosis as static venous blood deoxygenates
RED -> Reactive hyperaemia
describe the color change in raynaud’s phenomenon
triphasic color changes
why are serum autoantibodies in autoimmune connective tissue disorders important
Useful diagnostically
Some correlate with disease activity
May be directly pathogenic
are arthralgia and arthritis erosive
no
is male or female more common in SLE
female
9:1 ratio
typical onset of age of SLE
15-45
in SLE, do X-ray show bony erosiion
no
typical clinical features of SLE
swan neck deformity
arthritis and deformity of fingers
causes of deformity in SLE
soft tissue damage
swan neck deformity is characteristic of which RA
SLE
skin and mucosa clinical features of SLE
Skin and mucosa:
Malar rash – erythema that spares the nasolabial fold
Photosensitive rash
Mouth ulcers
Hair loss
vascular clinical features of SLE
raynaud’s phenomenon
MSK clinical features of SLE
arthralgia
arthritis
usually non-erosive
haematological clinical features of SLE
autoimmune thrombocytopenia (low platelets)
haemolytic anaemia
Lymphopenia
systemic clinical features of SLE
renal disease(glomerulonephritis)
cerebral disease
serositis
myocarditis
is lymphadenopathy clinical features of SLE
yes
which antibody can be found in SLE (2)
anti-nuclear antibodies (ANA)
antiphospholipid antibodies(APL)
is ANA found in all SLE patients
yes, so absence of ANA rules out SLE
but ANA not specific to SLE
what antibodies can be present in SLE (5)
Anti-ds-DNA antibodies
Anti-Ro
Anti-La
Anti-Smith (Sm)
Anti-RNP
what are APL (antiphospholipid)antibodies associated with increase risk of
thrombosis (arterial – stroke, venous – DVT)
pregnancy loss
what does Persistent presence of APL + a clinical event mean
anti-phospholipid antibody syndrome
what is primary anti-phospholipid antibody syndrome
Anti-phospholipid antibody syndrome absence in SLE
which antibodies are specific to SLE
anti-dsDNA
Anti-Sm
which antibodies in SLE are specific to SLE and serum level correlates to disease activity
anti-dsDNA
which antibodies in SLE are specific to SLE and serum level DONT correlates to disease activity
anti-Sm
which immunopathology in SLE is innate immunity (2)
Overactivity of type 1 interferon pathway
Complement pathway abnormalities
which immunopathology in SLE is adaptive immunity
autoreactive B & T cells
in SLE how did immune system generate a response to nuclear antigen
- Apoptosis leads to translocation of nuclear antigens to membrane surface
2.Impaired clearance of apoptotic cells results in enhanced presentation of nuclear antigens to immune cells - B cell autoimmunity
- Tissue damage by antibody effector mechanisms e.g. complement activation and Fc receptor engagement
what is the hypothesis called in SLE to describe the stimulation of immune system to generate a response to nuclear antigen
waste disposal hypothesis
what are the key investigations to do in SLE
bloods
urine
imaging
blood results in SLE
high ESR
normal CRP (unless infection/serositis/arthritis)
why need to check urine in SLE
glomerulonephritis
urinalysis + quantify urine protein:creatinine ratio
what are some immunological findings to test for in SLE
Antinuclear antibodies (ANA)
Anti-dsDNA antibodies
Complement consumption – e.g. low C4 and C3
antiphospholipid antibodies (APL)
relationship of complement C3 and C4 and anti-dsDNA in SLE patients
when C3 & C4 reduce
anti-dsDNA increase
kidney findings to test for SLE
creatinine in blood
creatinine in urine
eGFR
protein in urine
Protein:Creatinine ratio (PCR)
CKD EPI
albumin in blood
haemological findings to test for SLE
Hb
platelet
lymphocyte
reticulocyte
what are the treatment goals in SLE
remission or low disease activity and prevention of flares
Balance of controlling disease vs avoiding iatrogenic harm (especially steroids)
steroids side effects when treat SLE
Infection
Osteoporosis
Avascular necrosis (AVN) - often affects hips: higher incidence in lupus, especially in presence of APL Abs
medication for mild SLE
Hydroxychloroquine (main)
steroids for acute flare (but aim withdraw asap)
medication for serious SLE
immunomodulatory agents (mycophenolate, methotrexate, azathioprine)
medication for SLE + kidney disease
Mycophenolate +/- rituximab
SLE B-cell targeted therapies
Rituximab = anti-CD20 monoclonal antibody: depletes B cells
Belimumab = anti-BAFF antibody (BAFF = a B cell survival factor/cytokine)
myocarditis + SLE medication
iv steroids + iv cyclophosphamide (+/- rituximab)
Patients with SLE and antiphospholipid antibody syndrome medications
anticoagulation (warfarin)
what is an emerging therapy for SLE
anifrolumab (interferon receptor blockade)
what needs to be considered when treating SLE women with pregnancy
Consider both risk of disease & drugs to both mother and to fetus
aim get to remission first
medical treatment for SLE pregnant women
Hydroxychloroquine, azathioprine, low molecular weight heparin (LMWH) safe
which antibody in SLE can cause miscarriage
APL
what medication can help reduce miscarriage risk in SLE
aspirin or heparin
where are heberden’s nodes
at DIPJ
where are bouchard’s nodes
at PIPJ
if we see symmetrical small joint polyarthritis affecting DIPJs and PIPJs, and patient’s hand cannot grip properly, what’s likely diagnosis
OA
treatment for OA
analgesia
hand therapy
are there any disease modifying therapy for OA
no
raynaud’s phenomenon is a characteristic of what disease
SLE
positional chest pain in context of SLE is what
might suggest pericarditis
may come from soft tissue pr ribs
pain on inspiration in context of SLE implication
maybe pulmonary embolism as SLE patients have APL antibodies which predispose them to thrombosis
urine tests in SLE
urinalysis (urine dip)
UPC ratio to quantify proteinuria
bloods in SLE (need test what)
FBC
ESR, CRP
ANA, APL antibodies
complements C3 and C4
imaging for SLE
CXR ( look for pleural effusion, enlarged contour of heart if large pericardial effusion)
echocardiogram (look for pleural effusion)
CT pulmonary angiogram
symmetrical polyarthritis affecting both large and small joints suggest what
RA
lupus (so needa check antibodies)
is arthralgia or arthritis more common in SLE
arthralgia
RA treatment
DMARDs(disease modifying antirheumatic drugs) eg methotrexate, hydroxychloroquine)
short course of oral steroids for acute inflammation but avoid long term steroids
how many bones do a child skeleton has
270
how many bones do adult hv
206
where do long bone growth occurs post-natally
physis (at proximal and distal end)
bone development step for flat bone
intramembranous mesenchymal cells –> bone –> flat bones
bone development step for long bone
endochondral mesenchymal –> cartilage –> bone –> long bones
steps for intramembranous ossification
- condensation of mesenchymal cells then differentiate into oesteoblasts where ossification centre forms
- secreted osteoid traps osteoblasts which become osteocytes
- trabecular matrix and periosteum form followed by angiogenesis
- compact bone develops superficial to cancellous bone
- crowded blood vessels condense into red bone marrow
how many ossification centre do endochondral ossification involve
2
primary and secondary
does flat bone formation involve 1 or 2 ossification centre
1
does long bone formation involve 1 or 2 ossification centre
2
what is primary ossification centre
Sites of pre-natal bone growth through endochondral ossification from the central part of the bone
what is secondary ossification centre
Occurs post-natal after the primary ossification centre and long bones often have several (the physis)
steps for endochondral primary ossification formation
- mesenchymal differentiation at primary ossification centre
- cartilage model of future bony skeleton forms
- angiogenesis, capillaries penetrate cartilage
- calcification at primary ossification centre to form spongy bone
- perichondrium transform into periosteum
- cartilage and chondrocytes continue to grow at ends of bone to form secondary ossification centre
where does post bone growth happen
secondary ossification centre (physis)
what are the 6 parts at growth plate / physis
- growth plate zones
- reserve zone
- proliferative zone
- maturation and hypertrophy
- calcified matrix
- zone of ossification
what happens at the growth plate/ physis
- Zone of elongation in long bone
- Contains cartilage
- Epiphyseal side – hyaline cartilage active and dividing to form hyaline cartilage matrix
- Diaphyseal side – Cartilage calcifies and dies and then replaced by bone
where do prenatal bone growth occur
primary ossification centre
in what 4 ways are children’s skeleton differ to adult
- elasticity
- physis
- remodelling potential
- speed of healing
why children’s bone can bend more than adult
have a higher proportion of cartilage and collagen
why children bone more prone to plastic deformity, buckle fracture, greenstick injury
higher density of haversian canals
which 3 injuries are children more prone to
plastic deformity(bends before break)
buckle fracture(compress out)
greenstick injury (like a tree)
when does growth of physis stop for girls and boys
Girls 15-16
Boys 18-19
what are the classification for physeal injuries
salter-harris
what can physeal injury lead to
growth arrest, then deformity
causes of physeal injury
trauma
tumor
chemo
what do speed of healing and remodeling potential of skeleton depend on
location and the age of the patient
physis at which part grows more (2)
knee
extreme of upper limb (shoulder/ wrist)
what are the 4 common children’s congenital conditions in skeleton fracture
- developmental dysplasia of hip(DDH)
- club foot
- achondroplasia
- osteogenesis imperfecta
what is developmental dysplasia of hip(DDH)
Group of disorder of the neonatal hip where the head of the femur is unstable or incongruous in relation to the acetabulum
what does normal development of femur relies on
the concentric reduction and balanced forces through the hip
describe the spectrum of DDH (3)
dysplasia – subluxation – dislocation
risk factors of DDH
Female
First born
Breech
FHx
Oligohydramnios
Native American/Laplanders – swaddling of hip
Rare in African American/Asian
examination of DDH in baby
screening to check range of movement
investigation of DDH
USS (birth to 4 months)
Xray (after 4 months)
measure acetabular dysplasia and hip position
treatment for DDH
pavlik harness
what happens if failed pavlik harness when treating DDH
secondary changes to capsule and soft tissue
treat with MUA + Closed reduction and Spica
what is another name of clubfoot
Congenital Talipes Equinovarus
what is clubfoot/Congenital Talipes Equinovarus
congenital deformity of foot
risk factors of club foot
genetic
Highest in Hawaiians
M2:1F
what is the gene associated in Highest in clubfoot
PITX1 gene inactivation
mnemonic of deformity in Congenital Talipes Equinovarus / clubfoot
CAVE
what does CAVE stand for in deformity of Congenital Talipes Equinovarus
Cavus –high arch: tight intrinsic, FHL, FDL
Adductus of foot: Tight tib post and ant
Varus: Tight tendoachillies, tib post, tib ant
Equinous: tight tendoachilles
name and describe treatment for clubfoot
Ponseti method
1. First a series of casts to correct deformity
2. Many require operative treatment
, Soft tissue releases
3. Foot orthosis brace
4. Some will require further operative intervention to correct final deformity.
which is the most common skeletal dysplasia
achondroplasia
nature of achondroplasia
genetic
autosomal dominant
which gene mutation in achondroplasia
G380r mutation in FGFR3 (fibroblast growth factor receptor)
function abnormally, slowing down the growth of bone in the cartilage of the growth plate.
what happens in achondroplasia
inhibition of chondrocyte proliferation in theproliferative zoneof thephysis
results in defect in endochondral bone formation
which zone does achondroplasia affect in physis
proliferative zone
name of clinical presentation of achondroplasia
Rhizomelic dwarfism
what is Rhizomelic dwarfism
Humerus shorter than forearm
Femur shorter than tibia
Normal trunk
Adult height of approx. 125cm
Normal cognitive development
Significant spinal issues
what is another name of osteogenesis imperfecta
brittle bone disease
nature of osteogenesis imperfecta
Hereditary – autosomal dominant or recessive
which type of collagen in affected in osteogenesis imperfecta
decrease in type 1 collage
why is there decrease in type 1 collagen in osteogenesis imperfecta (2)
Decreased secretion
Production of abnormal collagen
consequence of reduced type 1 collagen
insufficient osteoid production
effects in bones in osteogenesis imperfecta
Fragility fractures
Short stature
Scoliosis (spine twists and curves to the side)
what are some non-orthopaedic manifestations in osteogenesis imperfecta
Heart
Blue Sclera
Dentinogenesis imperfecta – brown soft teeth
Wormian skull
Hypermetabolism
medical treatment for osteogenesis imperfecta
bisphosphonates (inhibit osteoclast)
denosumab (block RANKL to bind, inhibit osteoclast)
setrusumab
surgical rteatment for osteogenesis imperfecta
mechanical alignment
stabilisation
5 types of paediatric fractures (PAIDS)
pattern
anatomy
intra/extra-articular
displacement
salter-harris
5 types of pattern in paediatric fractures
transverse
oblique
spiral
comminuted (broken bone in at least 2 places)
avulsion (pulled off ligament)
how is anatomy of paediatric skeleton separated into 3 parts
proximal 1/3
middle 1/3 diaphysis
distal 1/3
*this is different to adult
is there callus formation in primary bone healing
no
steps in secondary bone healing
- haematoma formation
- fibrocartilaginous callus formation
- bony callus formation
- bone remodelling
what is primary bone ehaling
heals by direct union
what are the 2 bone healings in intra/extra articular fracture
primary and secondary bone healing
4 types of displacement in paediatric fracture
displaced
angulated
shortened
rotated
what are the 5 types of Salter Harris physeal injuries (SALT)
- (Physeal)Separation
- Fracture traverses physis and exits metaphysis (Above)
- Fracture traverses physis and exits epiphysis (Lower)
- Fracture passes Through epiphysis, physis, metaphysis
- Crush injury to physis
which type of salter harris is most common
type 2
what are keys of fracture in growth arrest
location
timing
2 types of injuries to physis in growth arrest
Whole physis – limb length discrepancy
Partial physis – angulation as the non affected side keeps growing
treatment for growth arrest
- limb length correction a9shorten long side or lengthen short side)
2, angular deformity (stop growth of unaffected side or reform bone via osteotomy)
main aim of growth arrest treatment
Minimise angular deformity
Minimise limb length difference
the 4 Rs in fracture management
- resuscitate
- reduce
- restrict
- rehabilitate
2 types of reducing fracture
open
closed
what is closed reduction in treat bone fracture
Reducing a fracture without making an incision
example of bone reduction
traction
manipulation
what is open reduction in healing bone fracture
Making an incision
The realignment of the fracture under direct visualisation
aim of reduction in treating bone fracture
Correct the deformity and displacement
Reduce secondary injury to soft tissue / NV structures
main goal of restriction in bone healing
Maintain the fracture reduction
Provides the stability for the fracture to heal
Children rarely have issues with bone not healing
Can have issues with too much healing!
2 types of restriction in bone healing
external and internal
examples of external restriction in bone healing
splints
plaster
examples of internal restriction in bone healing
plate and screws
intra-medullary device
benefits of fast remodelling and high healing potential in children using external restriction
operative internal fixation often can be avoided
internal restriction in bone healing drawbacks
Operative intervention may be required
need Consider the ongoing growth at the physis
Metalwork may need to be removed in the future
what is a great rehabilitator in children bone fracture treatment
playing
what is limping child
difficulty in walking
4 types of limping child
septic arthritis
transient synovitis
perthes
SUFE
is septic arthritis in child an orthpedic emergency
yes
treatment for septic arthritis in child
wash out of joint to clear infection
what classification to score probability of septic arthritis in child
Kocher’s classification
components of Kocher’s classification to score probability of septic arthritis
Non weight bearing
ESR >40
WBC >12,000
Temperature >38
key history of septic arthritis in child
Duration
Other recent illness
Associated joint pain
if there is no high temp/ increase WBC and ESR, what type of limping in child can we exclude and consider what
septic arthritis
can consider transient synovitis
what is transient synovitis
inflamed joint in response to a systemic illness
treatment for transient synovitis
Supportive treatment with antibiotics is the treatment
investigations for septic arthritis
USS
XRay
MRI
what is perthes disease
Idiopathic necrosis of the proximal femoral epiphysis
age of perthes disease in child
4-8yo
treatment for perthes disease
supportive treatment
what has to be excluded first before diagnosing perthes diseaase
septic arthritis
investigation for perthes disease
Xray
male or female more common in perthes disease
male
full name of SUFE in limping child
Slipped upper femoral epiphysis
what is SUFE
proximal epiphysis slips in relation to the metaphysis
age of SUFE common
12-13 yo during rapid growth
what has to be excluded first before diagnosing SUFE
septic arthriti
treatment for SUFE
operative fixation to prevent further slip and minimise long term growth problems
imaging for SUFE
xray
