Orthopaedics and Rheum Flashcards
describing a fracture
complexity = simple (closed), compound (open)
type = fissure, impaction, greenstick, transverse, avulsion, comminuted, oblique, spiral
comminuation = number of pieces broken into
location
displacement = degree of movement of bone from normal location: Translation (sideways movement, as % of bone diameter), angulation (bend in degrees), and shortening (collapse, in cm)
FRAX
explain
fracture risk assessment score
estimates 10 year fracture risk with BMD for people 40-90
3 person, 3 frac, 3 put in, 2 conds 3 person = age, sex, BMI 3 frac = prev frac, parent hip frac, low fem neck BMD 3 put in = alc, smoke, glucocorticoids 2 conds = RA, secondary osteo
low risk: reassure and give lifestyle advice
intermediate risk: offer BMD test
high risk: offer bone protection treatment
5 most common fractures
important fractures
what to assess
5 most common clavicle arm wrist (colles') hip ankle
important fract
scaphoid
fem head
- both these can lead to avascular necrosis progressing to joint destruction and osteoarthritis
assess
mech of injury
sound/feeling of break
loss of function
wrist fractures
bones in wrist
3 types
mgmt
Scared lovers try positions that they can’t handle
[1] bottom next to thumb - Scaphoid, lunate, triquetrum, pisiform, [2] top next to thumb - trapezium, trapezioid, capitate, hamate
3 types
Colles’ (distal radius with dorsal displacement fragments)
Smith’s (distal radius with volar displacement)
Scaphoid (*vulnerable blood supply) - fall onto outstretched hand in 20-30yr olds
mgmt
Reduction via manipulation with anaesthesia
Immobilisation initially avoid full cast as swelling may impede circulation
scaphoid fracture sign
ix
mgmt
comp
tenderness in anatomical snuffbox
ix
difficult to view on XR so need 4 views!!
mgmt
Presumptive cast immobilisation (6-8 weeks) + repeat exam and XR at 10-14 days
comp
avascular necrosis - distal blood supply
what in anatomical snuffbox
radial nerve sensory branch
scaphoid bone
colles fracture what who patho appearance comp mgmt
what
distal fracture of radius +/- ulnar with dorsal displacement of fragments
who
fall with OA
patho
FOOSH with forced dorsiflexion of wrist
appearance onXR
dinner fork on lateral view
comp
median nerve damage
mgmt
reduction
immobilisation
smiths fracture what patho appearance comp
what
reverse colles: distal fracture of radius with volar
patho
fall backwards
appearance
garden spade deformity
comp
median nerve damage
NOF def why imp types causes RF pres ix grading mgmt mortality comps
def Proximal to 5cm below lesser trochanter
why imp
most common
types
Intracapsular #
- Femoral neck between edge of femoral head and insertion to capsule
- 50% (medial and lateral circumflex artery)
- May disrupt blood supply to femoral head - avascular necrosis
Extracapsular trochanteric # distal to insertion, involving or between trochanters
Extracapsular subtrochanteric # below lesser trochanter to 5cm distal
causes
Post minor trauma in elderly, osteoporosis, + metastatic disease
RF
falls - instability, lack of core strength, gait disturbance, sensory impairment, frax
pres pain in outer upper thigh or groin radiates to knee no weight bearing affected leg shortened, adducted and externally rotated loss of internal rotation in flexion
ix
FBC, crossmatch, renal, glucose, ECG
AP and lateral XR (Shenton’s line)
MRI if # suspected but not obvious on XR
grading
Intracapsular NOF - Garden’s 1 = incomp, 2 = comp not disp, 3 = comp disp <50%, 4 = comp, disp > 50%
mgmt
analgesia - NOT NSAID
surgery within 1 day
intracapsular undisplaced = internal fixation with screws
IC displaced = replace fem head with haemiarthroplasty OR total hip replacement
EC = dynamic hip screw
post replacement care = do not flex beyond 90 (use long handled shoe horn), do not cross legs (pillow between legs at night), exercise to strengthen hip abductors
mortality = 10% in 1 month, 33% in 3 months
comps infection haemorrhage avascular nec DVT pneumonia -> give dalte
why you get fem shaft fractures
high velocity
high energy
RTA
ankle factures joints pres when to XR views classification types mgmt monitor
joints
2 - where tibia and fibula meet talus + syndesmosis (tibia to fib)
true joint = tibiotalar, plantar, dorsiflexion
subtalar joint - talus and calcaneus - inversion/eversion
pres similar to severe sprain immed severe pain swelling (localised or along leg) bruising tenderness consider break if obvious deformity, inability to weight bear, bony tenderness
when to XR
ottawa ankle rules:
>55
inability to weight bear for +4 steps
bone tenderness at ost edge or tip of lateral malleolus/medial
(+XR midfoot) bone tenderness at base of 5ht metatarsal, cuboid or navicular
views
AP
lateral
oblique - 15 deg
class danis-weber
types
potts - Distal tibia and fibula (bimalleolar) - unstable and require urgent Rx
snowboarders - Lateral process of talus - by dorsiflexion and inversion
mgmt If neurovascular compromise or dislocation (obvious deformity) then reduce immediately (before XR, under sedation or analgesia) Reduce Stabilise (4-6 weeks) moulded cast Analgesia Elevation Re-assess neurovascular status
monitor
XR at reduction, 48 hours, 7 days, then 2 weekly
main worrying comp of fracture when worry mgmt when it happens for dx comp post mgmt treatment for that
COMPARTMENT SYNDROME
when worry
Pain out of proportion: 6Ps, pain, parasthesia, pallor, paralysis, perishingly cold
mgmt
prompt fasciotomy
when it happens
Post fracture or reperfusion
for dx
compartment pressures >20 = suggestive, >40 = diagnostic
comp
myoglobinuria -> RF
mgmt
aggressive IV fluids
fracture healing
time
stages
time 3-12 w phalange - 3w radius 4-6 humerus 6-8 NOF or femur 12
stages
- haematoma formation - hours
- fibrocartilaginous callus formation - soft callus = days (secrete collagen + proteoglycans)
- bony callus formation - weeks (direct bone formation)
- bone remodelling = months (organised cortical bone), continuously remodelled therefore no scarring
frozen shoulder joint affected patho age assoc classic pres mgmt
joint = glenohumeral
patho
Thickening and contraction of glenohumeral joint capsule ± formation of adhesions - pain and loss of function either spont or post rotator cuff injury
age
40-65
assoc
diabetes
thyroid
pres
LOSS OF EXTERNAL ROTATION
mgmt
analgesia - para/NSAID, tens, activity, physio
remodelling process of bone
Osteocytes send signal to osteoclasts and osteoblasts
Osteoclasts resorb bone matrix: resorption pit - increases serum Ca
Osteoclasts undergo apoptosis and send signals to osteoblasts
Osteoblasts synthesise bone matrix
Bone matrix undergoes mineralisation
what is RANK
RANKL expressed by osteoblasts interacts with RANK receptor on osteoclasts
OsteoProteGerin secreted by osteoblasts inhibits RANKL activation of RANK
what happens in post menopausal women to cause osteoporosis
mgmt
Overexpression of RANKL overrides inhibitory Osteoprotegerin
mgmt
bisphosphonates
Osteoporosis def who to assess locations patho pres RF meds for dx ix mgmt
def Skeletal disease characterised by low bone mass and micro-architectural deterioration leading to increasing fragility and fracture risk
who
all women >65 and men >75 should be asessed for it
younger and presence of RF:
prev #, steroids, falls, fh of NOF, secondary osteo, low BMI, smoke, alc
location
Spine (vertebral crush), wrist (distal radius), hip (proximal femur), pelvis
patho
Increased breakdown by osteoclasts
Decreased bone formation by osteoblasts
pres
asymp until frcture
loss of height
kyphosis
RF
SHATTERED + FRAX or QFracture + SEDENTARY
S = steroids + cushings (>7.5mg for 3m)
H = hyperth, hyperPTH, hypercalciuria
A = alc + tobacco
T = thin or AN
T = testosterone decreased - primary hypogonadism or anti-androgens @ PrCa
E = early meno <45
R = real/liver function - renal osteodystrophy in CKD, chronic liver disease
E= erosive/inflam disease (IBD), RA, MM, mets
D = dietary ca/T1DM - malabsorption, malnutrition
+ FAM HISTORY
meds steroids = Decrease Ca absorption from gut, Increase osteoclast activity, Decrease muscle mass PPI long term SSRI antiepileptics glitazones aromatase inhibs - letrozole
for dx
XR - often normal *nothing seen till lose 30% BMD
- Radiolucency, cortical thinning, biconcave vertebrae
DEXA - at proximal femur
Identify treatable causes and rule out differential Dx of myeloma
OTHERS to exclude:
**FBC, ESR, CRP
**U+E, LFT, TFT, serum Ca
Testosterone/gonadotrophins (in men), prolactin
Serum Ig, paraproteins, Bence Jones protein
**Bony profile: Ca, PO4, ALP, PTH, albumin
24 hour urinary cortisol/dexamethasone suppression test
Endomysial and/or tissue transglutaminase antibodies (coeliac disease)
Isotope bone scan
Markers of bone turnover, when available
Urinary calcium excretion
All normal at osteoporosis
mgmt
Lifestyle: smoking, alcohol, wt bearing exercise, balance (fall risk), calcium + vit D rich diet, fall prevention
Meds: Bisphosphonates (alendronate) + Ca + vit D supplements - AdCal D3, Accrete D3
Fall prevention: avoid polypharmacy
If low testosterone add testosterone
If intolerant bisphosphonates use denosumab (monoclonal aB to RANKL)
Raloxifene can be used for women if alendronate not tolerated (selective oestrogen receptor modulator)
explain dexa score expectation for osteoporosis
T-score < -2.5 (s.d. below young healthy adult mean)
-2.5 < T
Qfracture score
10 year risk of frag #
30-99 yr olds
includes larger RF group
e.g. cardiovascular disease, history of falls, chronic liver disease, rheumatoid arthritis, type 2 diabetes and tricyclic antidepressants
bisphosphonates
examples
mech
SE
examples
Alendronic acid, risedronate, zoledronic acid
mech
Inhibit osteoclastic bone resorption
SE
Upper GI therefore take sitting upright with plenty of water first thing before food - crap absorption (1 hour before food)
Difficulty swallowing, oesophagitis, gastric ulcers
Osteonecrosis of the jaw
what would these results diagnose:
- normal calc, phos, ALP, PTH
- decreased calc, phos, increased ALP, PTH
- increased calc, ALP, PTH decreased phos
- decreased calc, increased ALP, PTH, phos
- normal calc, phos, PTH and increased ALP
- oestoporosis
- ostemalacia
- primary hyperPTH
- CKD - secondary hyper PTH
- pagets
osteomalacia what is it rickets what is it mech RF causes pres rickets + osteomalacia low phos symps ix mgmt
osteo = Disorder of mineralisation of bone matrix (osteoid) after fusion of epiphyses
rickets = Disorder of mineralisation of bone matrix prior to fusion of epiphyses
SOFT BONES
mech
Vitamin D deficiency leads to low calcium and phosphate
Low Ca and PO4 leads to secondary hyperparathyroidism
RFs
Dark skin, old/young, pregnancy, obesity, alcohol, vegetarianism, poverty, fam Hx
casues
1. Lack of sunlight, lack of adequate diet
2. GI malabsorption: surgery, short bowel, pancreatic disease, CF, CD, coeliac
3. Renal disease: -> defective 1,25 form = renal osteodystrophy
4. Liver disease: -> cirrhosis
5. Drugs: anticonvulsants, rifampicin (liver, stop 25-hydroxy)
6. Rare:
Tumour induced hypophosphataemia (FGF-23 - hyperphosphaturia)
Fanconi syndrome (proximal renal tubule dysfunction)
Renal tubular acidosis
7. Genetic:
rickets pres
Leg bowing - genu varum
Knock knees - genu valgum
In first few months: craniotabes (softening of skull), frontal bossing, rachitic rosary (enlarged end segment ribs) -> rachitis lung
Dental abnormalities (enamel)
Delayed walk/waddling gait, impaired gait
Symptoms of hypocalcaemia: convulsions, irritable, tetany, apnoa, cardiac arrest
osteomalacia pres
Widespread bone pain + tenderness (low back pain and hips)
Proximal muscle weakness - waddling gait (if severe)
Fatigue
Symptoms of underlying disease
Costochondral swelling, spinal curvature, hypocalcaemia (tetany, carpopedal spasm - trousseau sign and chvostek)
low phos symps
muscle weakness
parasthesia
ix
Serum 25-hydroxyvitamin D - low
Renal function, electrolytes, LFT, PTH
Ca: low, PO4: low (generally at renal phosphate wasting), PTH: high, ALP: very high
FBC: anaemia if malabsorption
Urinary calcium - low, urinary phosphate - high
XR - *Looser pseudofractures with sclerotic borders (parallel) - bilateral at femoral neck
DEXA - low BMD
Iliac crest biopsy - failed mineralisation
mgmt
Ca + Vit D - (CaCO3 + cholecalciferol) e.g. accrete
Monitor Ca regularly for a few week
source of vit d
90% sunlight, dietary - oily fish, liver, egg yolks, fortifited cereals (not dairy)
vit d physiology
Cholecalciferol (D3) -> liver = 25 hydroxyvitamin D3 (inactive circulating) -> kidney = 1,25 dihydroxyvitamin D3 (active hormone)
To bone: increases Ca mobilisation, increases osteoclast function
To intestine: increases Ca absorption, increases PO4 absorption
To PTG: decreases PTH
PTH physiology
Low Ca -> increased PTH
To bone -> increase osteoclast function
To kidney -> increases 1,25vD3 (1-alphahydroxylase), + decreases Ca excretion + increases PO4 excretion
pagets disease of the bone def where genetic pres comp assoc ix mgmt
def
Increased turnover of bone
Lytic phase - increased bone resorption by osteoclasts
Sclerotic phase - *Rapid bone formation by osteoblasts: disorganised and mechanically weaker and deformity/larger.
where
axial skeleton: lumbosacral spine, pelvis, skull, femur, tibia
gene
AD SQSTM1 mutation
pres
asymp
classically - older male with bone pain and isolated raised ALP
bone pain + deformity with increased skin temp
pain at night
comp
Bone pain
Deformity: sabre tibia, kyphosis, skull bossing, enlarged maxilla/jaw
Pathological fracture (heavy bleeding as v.vascular)
Deafness/tinnitus compression of CN 8 by ear ossicles
Increased vascularity may lead to high output cardiac failure
assoc
osteosarcoma
ix ALP - high ca, phos, PTH normal XR - Osteolysis and osteosclerosis (lytic and scleortic lesions), *Blade of grass lesion between healthy and sclerotic long bone, Cotton wool pattern of multifocal sclerosis in skull isotope bone scan
mgmt
Control pain and reduce or prevent progression
Pain: NSAIDs and paracetamol
Antiresorptive: bisphosphonates
N.b. IV may give flu-like symptoms
Zoledronate popular as good with single IV dose
Monitor ALP
causes of joint pain
differences between inflam, degen, and which joints
causes
ARTHRITIS
others = reactive arthritis, tendon/muscle damage, hyperuricaemia, referred pain, immune (e.g. SLE), tumour, ischaemia, sponyloarthtitides
inflam = Ease on use, worse in morning (>60 mins), hot and red, responds to NSAIDs, swelling *synovial and bony, young/psoriasis/fam Hx
deg = Worse with use, morning (<30 mins), mainly evening, prior occ, sport, *no swelling, not inflamed
which joints -
OA - distal interphalageal
RA = MCP, MTP, PIP
inflammation
acute phase proteins examples
ESR increases with?, phase, how works
CRP increases with? phase, how works, imp negs
Levels fluctuate wrt injury e.g. trauma/MI/burns
exampls
CRP, ESR, fibrinogen, ferritin, C3/C4, caeruloplasmin etc.
ESR
Increases with inflammation and infection. More fibrinogen produced, RBCs crosslinked and sediment quicker. Affected by RBC shape and number
<22mm/Hr (men), <29mm/Hr (women)
also increases with… Age, sex, drugs e.g. steroids, obesity (fat produces IL-6)
Slow on, slow off: peak at 7 days
CRP
Acute phase protein which increases in inflammatory conditions, connective tissue disorders, neoplastic disease and infection (esp bacterial)
Quick on, quick off - peak at 1 day, normal at 7 days
SLE, OA, UC
Binds to damaged cells and activates complement, phagocytosis by M
osteoarthritis def patho common joints rfs dx - triad pres classic XR other ix ddx mgmt
def Clinical syndrome of joint pain + functional limitation + reduced QoL
patho
Deterioration of *articular cartilage and formation of new bone - osteophytes at joint margins
common joints knees hips small joints hands spine
rfs
Age, female sex, obesity, occupation/hobbies, genetic (50%), joint laxity
dx triad
Aged > 45 + activity related jt pain + no morning stiffness (<30 minutes)
pres
Jt pain exacerbated exercise + relieved rest, stiffness after rest (gelling), reduced function
Joint swelling/synovitis - warmth + effusion
Reduced ROM
Crepitus
Pain on movement *may lead to disuse atrophy and weakness
Bony swelling and deformity - osteophytes: DIP (Heberden’s) + PIP (Bouchard’s)
squaring of the thumbs - fixed adduction
No systemic features
classic XR LOSS Loss of joint space Osteophytes Subchondral/subarticular sclerosis Subchondrial cysts
other ix
bloods - normal
joint aspiration - ?SA/gout
RF + ANA negative
ddx hip + knee = bursitis referred pain gout all arthritis
mgmt
Patient education, weight loss, screen depression, *exercise for muscle strength, aids and devices (walking sticks, tap turners)
Local analgesia: topical NSAID for knee or hand + para (first line)
+ oral NSAID +/- PPI, opioids, capsaicin cream , intrarticular steroids - methylpred (2)
non-pharmacological treatment options include supports and braces, TENS and shock-absorbing insoles or shoes
For persistent pain affecting QoL:
Replacement (arthroplasty), fusion (arthrodesis)
pathogenesis of OA joints
Failure to maintain homeostasis of cartilage matrix synthesis and degradation
Synovial inflammation - IL1/6/TNF stimulates chondrocyte production
Chondrocytes produce increased MMP (matrix metalloproteinases e.g. collagenase) catalyse collagen and proteoglycan degradation
Increased catabolic cytokines (IL-1), loss of anabolic CKs (IGF-1)
Cartilage loss -> decreased joint space -> increased stress on subchondral bone
Microfracture, new bone (sclerosis) and synovial fluid seep (cysts)
surgical techniques in OA hip post op recovery advice to minimise risk of hip replacement dislocation comps
hip - cemented hip replacement, uncemented, sometimes hip resurfacing over femoral head
recovery
physio
home exercises
walking sticks/crutches - 6w
advise avoiding flexing the hip > 90 degrees avoid low chairs do not cross your legs sleep on your back for the first 6 weeks
comps
wound and joint infection
thromboembolism - LMWH for 4w post op
dislocation
OA vs RA xrays
OA LOSS Loss of jt space Osteophytes Subchondral cysts Subchondral sclerosis
RA LESS Loss of jt space Erosions Softening of bones (osteopenia) Soft tissue swelling
Rheumatoid arthritis def who main joints patho pres extra articular ix mgmt monitoring
def Chronic inflammatory autoimmune disease characterised by inflammation of synovial joints leading to joint and periarticular tissue destruction
who
40/50 yr old women
main joints
HANDS + FEET
patho
INFLAMMATION OF SYNOVIUM:
1. Increased angiogenesis, influx inflammatory cells + CKs, cellular hyperplasia
2. Cells (MP, TCells, plasma cells) release IL1/IL6/TNF - promote proliferation and MMP expression -> joint destruction
PROLIFERATION
1. Angiogenesis and hypertrophic synovium form pannus over articular cartilage
LOCALLY INVASIVE SYNOVIAL TISSUE
Pres
Active Symmetrical Polyarthritis >6w in 50 yr old woman
RHEUMATISM
RF+ve (80%), radial deviation wrist
HLA DR(rheumatism) 1/4
ESR/extra-articular e.g. restrictive lung disease/nodules
Ulnar deviation fingers
Morning stiffness, MCP, MTP, PIP swelling
ANA +ve (30%), assoc AnkSpon/AI
T-cell (CD4) and TNF
Inflammatory synovial tissue, IL1/IL6
Swan neck, boutonniere, Z-deformity thumb, loss of knuckle valleys when making a fist
Muscle wasting hands
+ cervical spine instability - atlanto-axial joint subluxation
extra articular
Rheumatoid nodules @ extensor surface of tendons (palisade ring of MP and fibroblasts with necrotic core) and *lungs
Vasculitic lesions - commonly skin rashes, leg ulcers (@Feltys)
Pleuritic chest pain - pleuritis or pericarditis, effusion
Eye problems: secondary Sjogren’s: scleritis and episcleritis, oral dryness
Neurological: peripheral nerve entrapment, mononeuritis multiplex, atlanto-axial subluxation (C1,C2) - soft tissue swelling within rigid tunnel
Respiratory system: rheumatoid nodules, Caplan’s syndrome, pulmonary fibrosis
Anaemia of chronic disease
ix
RF - 70% +ve
Anti-CCP abs - 70%, very specific so more likely erosive
XR hands and feet - erosions + soft tissue swelling, loss of jt space, periarticular osteopenia, absent osteophytes, deformity, subluxation
FBC - (normochromic normocytic chronic dis)
ANA (+ve 30%)
ESR/CRP raised
ferritin high, Pt high (reactive thrombocytosis)
U/E , LFTs
mgmt
Physiotherapy, OR, psych services (depression), podiatry
First line:
one DMARD (not working, increase dose)
Second Line if not winning >6m: Combination DMARD (with *methotrexate)
Choice DMARD = methotrexate or sulfasalazine or leflunomide
Adjunct - bridging treatment if really active to get under control: corticosteroid (low dose pred) + NSAID (lowest effective dose) short term
If not winning >1 yr: biologicals (expensive)
monitoring DAS28 (disease activity score) <3.2 = well controlled, >5.1 = active + CRP at each visit
rheumatoid lung
how many have it
symps
types
30%
symps
dyspnoea, cough, wheeze
types
- interstitial lung disease - often middle age men with dry cough and dyspnoea, mgmt corticosteroids
- rheumatoid nodules - benign but lead to pleural effusion
- caplans - assoc with coal workers pneumoconiosis (massive fibrosis) - well rounded nodules at lung periphery
- methotrexate pneumonitis - not common, cough, dyspnoea, fever
feltys syndrome
triad
+ other symps
TRIAD
RA, neutropenia, splenomegaly
+ leg ulcers, brown pigment of legs, lymphadenopathy
rheumatoid hands
palmar erythema wasting of thenar eminence - carpal tunnel sydnrome fixed flexion contracture swan neck button hole z thumb
due to rheumatoid tenosynovitis
explain anatomy of boutonneire deformity
and swan neck
boutonneires
rupture of central slip but lateral slips intact
finger pushes up
swan neck
rupture of lateral slip of extensor expansion, so proximal pharyngeal joint is extended
when they say examine hands where else should you look?
elbows and ears
ears for gouty tophus and elbows can have rheumatoid nodules
what is rheumatoid factor
IgM against your own IgG
lots of normal people have it
high titres assoc with progressive disease
what is seronegative rheumatoid
identical to sero posi but unlikely to have nodules or extra articular features
no IgM just IgG
40% hve antibodies to CCP - if so more progressive
methotrexate administration bits and bobs adverse effects excretion inhibs by CI monitoring
once per week
with folic acid on a non-MTX day
adverse effects
bone marrow suppression
renal and liver tox
pneumonitis/pulm fibrosis
excretion inhibs by - NSAIDs
CI
trimethoprim
monitoring
FBC, eGFR, LFT every 4-6 weeks in first year
what need to do prior to prescribing biological
tuberculin skin test or interferon gamma release assay
chest radiograph
hep B,C, HIV serology
treat latent TB
warn significant risk of serious infection
what is atlanto-axial subluxation
top of cervical spine is held together by tendons which can be weakened by rheumatoid tenosynovitis
if the odontoid peg subluxes backwards over days and weeks -> compress upper cervical cord causing progressive spastic tetraparesis
if compression is sudden - a rapid output of inhibitory impulses down vagus can cause cardiac arrest
so preoperatively I would arrange a lateral upper cervical radiograph in gental flexion
