Musculoskeletal Flashcards
Rheumatoid arthritis (RA)
a chronic systemic inflammatory autoimmune disorder that primarily affect the joints but may also manifest with extra articular features e.g. rheumatoid nodules or pulmonary fibrosis
Epidemiology of rheumatoid arthritis (RA)
affects ~1% of the population
more commonly seen in women (2-4x)
peak age of onset 30-50 yrs
Risk factors for rheumatoid arthritis (RA)
smoking*
genetic predisposition (HLA-DR4, HLA-DR1)
obesity
Family history of RA
Arthritic presentation of rheumatoid arthritis (RA)
Polyarthritis:
symmetrical pain, swelling, heat, stiffness (stiffness worse in morning lasting >30min) of affected joint
usually affects metacarpopahryngeal (MCP) / proximal interphalangeal (PIP) / metatarsopharyngeal (MTP) joints, later progressing to affect larger joints
Joint deformities (later in disease):
swan neck deformity (PIP hyperextension, DIP flexion)
boutonniere ferocity (PIP flexion, DIP hyperextension)
Z deformity of thumb (hyperextension of interphalangeal joint, fixed flexion of MCP)
ulnar deviation of fingers
atlantoaxial subluxation
piano key sign (dorsal subluxation of ulna)
NB Distal interphalangeal joints (DIP) are really affected, DIP involvement usually indicates psoriatic arthritis
extra articular manifestations of rheumatoid arthritis (RA)
Rheumatoid nodules:
skin (non tender firm swellings)
lungs (bilateral & peripheral)
Lungs:
pleuritic chest pain, fibrosis
Eyes:
keratoconjunctivitis sicca (most common)
episcleritis, scleritis
anaemia carpal tunnel syndrome purpura vasculitic ulcers Raynauds phenomenon (recurrent vasospasm of fingers & toes)
Examination findings for rheumatoid arthritis (RA)
compression test (Gaenslen squeeze test) = painful compression of MCP joint
may present as painful handshake
Investigation findings for rheumatoid arthritis (RA)
ESR/CRP (↑)
FBC (normochromic normocytic anaemia + thrombocytosis)
LFTs (↑ALP, ↑ gamma GT)
Rheumatoid factor (+ve in 70% of pts)
Antinuclear antibody - ANA (+ve in 30% of pts)
anti-cyclic citrullinated peptide (anti-CCP) antibody (+ve in 70% of pts)
synovial fluid analysis (cloudy, yellow appearance, leucocytosis (WBC = 5000-50,000) ↑proteins)
X-rays (early = loss of joint space, juxta-articular osteoporosis, soft tissue swelling, late= periarticular erosions, subluxation, bon/cartilage erosion, suchondral cysts)
USS (synovitis)
Imagine findings for rheumatoid arthritis (RA)
X-rays:
early = loss of joint space, juxta-articular osteoporosis, soft tissue swelling
late= periarticular erosions, subluxation, bon/cartilage erosion, suchondral cysts
USS; synovitis
Disease severity score for rheumatoid arthritis (RA)
DAS28
Diagnostic criteria for rheumatoid arthritis (RA)
≥6 points is considered RA
Joint distribution: 1 large joint = 0 points 2-10 large joints = 1 point 1-3 small joints = 2 points 4-10 small joints = 3 points >10 joints (at least 1 small) = 5 points
Serology:
negative RF & anti-CCP = 0 points
low positive RF or anti-CCP = 2 points
high positive RF or anti-CCP = 3 points
Duration:
< 6 weeks = 0 points
> 6 weeks - 1 point
Acute phase reactants:
normal CRP/ESR = 0 points
↑ CRP/ESR = 1 point
Antibodies for rheumatoid arthritis (RA)
Rheumatoid factor (+ve in 70% of pts)
Antinuclear antibody - ANA (+ve in 30% of pts)
anti-cyclic citrullinated peptide (anti-CCP) antibody (+ve in 70% of pts)
anti-CCP is most specific
Non drug management of rheumatoid arthritis (RA)
MDT approach
exercise
pain clinics
Pharmacological management rheumatoid arthritis (RA)
Symptomatic treatment:
NSAIDs (e.g. ibuprofen, naproxen) or COX-2 inhibitors (e.g. celecoxib) + a PPI (e.g. lansoprazole)
Corticosteroids:
for short-term flare up management and short term bridging treatment when starting DMARDs
DMARDs:
1st line: Methotrexate + corticosteroids to bridge treatment
other options: hydroxychloroquine, sulfalazine, leflunomide
Biologicals:
if moderate/severe disease after >3 months of DMARDs
e.g. rituximab, TNF-inhibitors (e.g. adalimumab, etanercept)
Methotrexate
given once a week orally, usually co-precribed with folic acid
monitoring: FBC / LFTs / renal function
Side effects: myelosuppresion, liver cirrhosis, pneumonitis, teratogenic (i.e. do not get pregnant )
NB avoid NSAIDs on day of methotrexate dose
Hydroxychloroquine
no regular blood test required
considered safe in pregnancy
side effects: retinopathy (bullseye retinopathy), corneal deposits
Sulfalazine
safe in pregnancy
monitoring: FBC / LFTs / renal function
side effects: interstitial lung disease, oligospermia, Heinz body anaemia, rash
Leflunomide
monitoring: FBC / LFTs / renal function / BP&weight
side effects: cushingoid features, osteoporosis, impaired glucose tolerance, HTN
Felty’s syndrome
complication of rheumatoid arthritis
triad of RA, splenomegaly, neutropenia
only seen in seropositive RA
treat firstling with methotrexate
Caplan syndrome
complication of rheumatoid arthritis in combination with pneumoconiosis (e.g. asbestosis/silicosis)
rapid development of basilar nodules & obstruction of ventilation
usually seen with coal dust exposure
Occular complications of rheumatoid arthritis
dry eye syndrome (keratoconjunctivitis sicca)
episcleritis
scleritis
steroid induced cataracts
Other complications of rheumatoid arthritis
osteoporosis respiratory (bronchiolitis, pulmonary fibrosis, pleural effusion, pulmonary nodules, bronchiolitis) raynauds phenomenon depression amyloidosis carpal tunnel syndrome vasculitis & vasculitic ulcers atlanta axial subluxation (due to inflammatory destruction of ligaments )
Raynaud phenomenon
characterised by paroxysmal vasospasm & subsequent vasodilatory chain of events affecting peripheral arterioles usually in the hands & feet
typically presents in young women
triggers: cold, emotional stress
Aetiology of raynauds
primary = raynauds disease:
onset usually <30y/o
secondary = raynauds phenomenon
may be related to RA, SLE, scleroderma, meds (COCP)
usually later onset in RA/SLE, >40 y/o
Presentation of Raynauds
usually symmetrical ischaemic phase (white) = vasoconstriction → hypoxic phase (blue) → hyperaemic phase (red) = vasodilation affects fingers & toes lasts 15-30 min after removing trigger no tissue damage / ulceration in primary
Management of Raynauds
avoid triggers
1st line: Nifedipine
2nd line: IV prostacyclin (lasts weeks to months)
Polymyalgia rheumatica (PMR)
inflammatory condition of unknown cause
generally affects people ~70y/o, more common in women
usually seen in pts of northern european descent
associated with HLA-DR4 & giant cell arteritis (10% of PMR pts have GCA)
Presentation of polymyalgia rheumatica (PMR)
usually rapid onset (,1 month)
fatigue, malaise, weight, polyarthralgia
morning stiffness (>45min)
symmetric pain/aches of shoulders/pelvic girdle/neck
no weakness
Investigating polymyalgia rheumatica (PMR)
ESR & CRP (↑) (ESR >50mm/h)
negative Rheumatoid factor
no autoantibodies
USS (bursitis of affected joint)
Management of polymyalgia rheumatica (PMR)
low dose corticosteroids e.g. 15mg prednisolone (typically dramatic response to steroids)
NB if no response to steroid consider alternative diagnosis
Giant cell arteritis (GCA) / temporal arteritis
Type of large vessel vasculitis
granulomatous vasculitis of large & medium sized arteries primarily affecting branches of the external carotid arteries, most commonly the temporal artery
most common form of systemic vasculitis in adults
Epidemiology of giant cell arteritis (GCA)
most commonly seen in northern european populations
typical onset >50y/o
more common in women (2-3x)
commonly associated with polymyalgia rheumatica (up to 50% of GCA pts have PMR)
Presentation of giant cell arteritis (GCA)
usually rapid onset (<1 month) headache (temporal/occipital) scalp tenderness unexplained facial pain jaw claudication vision loss/abnormality, diplopia, amaurosis fugax abnormal temporal artery on palpation
Investigations for giant cell arteritis (GCA)
ESR & CRP (↑)
FBC (normochromic normocytic anaemia)
Temporal artery biopsy (gold standard)
temporal artery USS (halo sign, wall thickening, stenosis)
Management of giant cell arteritis (GCA)
1st line: glucocorticoids e.g, prednisolone (give even if negative biopsy but GCA suspected)
+prophylaxis against side effects of long term steroid use e.g. bone protection
NB if no response to steroids, reconsider diagnosis
urgent ophthalmological review (visual loss often irreversible)
Sjogren syndrome
systemic autoimmune condition with lymphocytic infiltration of exocrine glands
Types:
primary = idiopathic, associated with HLA-DR52
secondary (~60% of cases) = associated with RA, SLE, systemic sclerosis, primary biliary cirrhosis
onset usually age 30-40 yrs
~10x more common in women
↑ risk of lymphocytic malignancy (MALT lymphoma)
Sjogren syndrome presentation
Xerostomia (dry mouth) xerophthalmia (dry eyes) keratoconjunctivitis sicca vaginal dryness & dyspareunia dental carries faitgue arthrlagia recurrent parotitis nasal dryness raynauds
Sjogren syndrome investigations
ESR (↑) Rheumatoid factor - RF (+ve in 50%) Antinuclear antibody - ANA (+ve in 70%) anti La - SSB (+ve in 30%) anti Ro - SSA (+ve in 70%)
Schirmers test (quantitatively measures tears) = +ve (<5mm of paper in 5 min)
salivary gland biopsy (focal lymphocytic infiltration)
USS of parotid glands
Sjogren syndrome antibodies
Rheumatoid factor - RF (+ve in 50%)
Antinuclear antibody - ANA (+ve in 70%)
anti La - SSB (+ve in 30%)
anti Ro - SSA (+ve in 70%)
Sjogren syndrome management
Symptomatic treatment:
artificial tears, artificial saliva, regular dental hygiene
pilocarpine (muscarinic agonist) = ↑ saliva & tear production
Antiphospholipid syndrome
autoimmune disorder with ↑ risk of thrombosis as a result of procoagulatory antibodies causing a hypercoaguable state
may be:
primary = idiopathic, associated with HLA-DR7
secondary = associated with SLE, RA, neoplasms
more common in females, usually seen young, fertile women
Antiphospholipid syndrome presentation
recurrent thrombotic events (DVT/PE/livido reticular/sinus thrombosis/stroke/TIA/MI)
recurrent miscarriages/premature birth/IUGR/pre-eclampsia
pulmonary hypertension
thrombocytopenia
arthralgia
splinter haemorrhages
Antiphospholipid syndrome investigations
antiphospholipid antibodies (aPL) / Lupus anticoagulant / anticardiolipin antibodies (on 2 occasions ≥12 weeks apart)
FBC (thrombocytopenia, haemolytic anemia)
clotting (↑APTT)
USS for DVT
MRI/CT (for CVD & PEG)
Antiphospholipid syndrome management
lifestyle modifications
acute management: LMWH/UFH
thromboprophylaxis: low dose aspirin (primary), or warfarin (secondary)
low dose LMWH in pregnancy if ≥pregnancy losses
Ankylosing spondylitis
a type of seronegative spondyloarthropathy, a chronic inflammatory disease of the axial skeleton leading to partial / complete fusion & rigidity of the spine
Epidemiology of Ankylosing spondylitis
peak onset 20-30yrs
3:1 male:female ratio
NB women tend to have milder, subclinical disease
Genetics of Ankylosing spondylitis
strong family tendency (~90% of disease inherited genetically)
associated with HLA-B27
Presentation of Ankylosing spondylitis
back & neck pain (gradual onset, dull pain, slowly progressive)
morning stiffness (improves with activity)
tender sacroiliac joints & buttock pain
↓ mobility of spine (↓ lateral & forward flexion)
↓ chest expansion
enthesitis (especially of achilles tendon)
unilateral anterior uveitis
fatigue
↓ lumbar lordosis
Investigations for Ankylosing spondylitis
pelvic X-ray (sacroilitis = subchondral erosions, sclerosis)
CRP/ESR (↑)
HLA-B27 (+ve)
Spine X-ray (bamboo spine, single central radio dense line (dagger sign), squared vertebral bodies, bony bridges between adjacent vertebrae, syndesmophytes)
Imaging findings for Ankylosing spondylitis
Spine X-ray (bamboo spine, single central radio dense line (dagger sign), squared vertebral bodies, bony bridges between adjacent vertebrae, syndesmophytes)
pelvic X-ray (sacroilitis = subchondral erosions, sclerosis)
Chest X-ray (apical fibrosis)
MRI/CT
Management of Ankylosing spondylitis
1st line: physiotherapy & NSAIDs
2nd line: TNF-alpha inhibitors or DMARDs e.g. sulfalazine if peripheral arthritis
complications of Ankylosing spondylitis
osteoporosis
cardiac problems e.g. aortic regurg
lung problems e.g. apical fibrosis, restrictive pulmonary disease
Psoriatic arthritis / psoriatic arthropathy
chronic inflammatory joint disease associated with psoriasis, its a seronegative inflammatory arthritis
~80% of its have preceding arthritis
most common in middle age, 35-55 yrs
associated with HLA-B27/B17/DR4/DR7
Presentation of psoriatic arthritis
most common presents as asymmetric oligoarthritis mainly affecting DIP & PIP joint with possible spinal involvement (sacroilitis)
enthesitis (mainly achilles tendon & plantar fascia)
tenosynovitis
dactylics (single digits, inflammation & swelling)
nail changes (pitting, yellowing, onycholysis)
history of scalp/nail problems
psoriasis
NB DIP involvement is indicative of psoriatic arthritis
Investigating psoriatic arthritis
X-rays of hands & feet (asymmetrical bony erosions, DIP/PIP involvement)
ESR/CRP (↑)
synovial fluid aspirate (no crystals, ↑ WCC)
CASPAR criteria (to diagnose psoriatic arhtirits)
Management of psoriatic arthritis
NSAIDs (if mild)
local corticosteroid injection
1st line: DMARDs (consider early in disease e.g. methotrexate (if significant cutaneous psoriasis) or leflunomide, sulfalazine)
2nd line: TNF-alpha inhibitors (inadequate control by DMARDs)
Gout
an inflammatory crystal arthropathy caused by the precipitation & deposition of uric acid crystals (monosodium rate crystals) synovial fluid & tissues
more common in men & older people (especially men aged 30-60yrs)
Risk factors for gout
male gender obesity HTN CHD CKD HF diabetes drugs (e.g. diuretics, chemo, cytotoxic drugs)
Presentation of gout
acute onset joint pain with a swollen/tender/erythematous joint (70% of first attacks/50% of all attacks affect 1st metatarsophalangeal (MTP) joint)
other joints affected include knee, wrist, ankles, elbows, small hand joints
tophi may be present (asymmetrical, chalky nodule under skin)
Investigations for gout
May be clinical diagnosis if typical presentation in 1st MTP
synovial fluid analysis (strongly negatively bifringent needle-shaped crystals under polarised light)
serum uric acid (>420 micro mol/L in men / >360micromol/L in women)
X-ray (periarticular erosions, punched out lesions, no periarticular osteopenia)
Synovial fluid analysis results for gout
strongly negatively bifringent needle-shaped crystals under polarised light
Management of gout
Acute attack:
1st line: colchicine & NSAIDs
2nd line: oral prednisolone (if colchicine & NSAIDs contraindicated e.g. Renal problems)
Chronic:
1st line: allopurinol (xanthine oxidase inhibitor)
2nd: febuxostat
Lifestyle modifications:
limit alcohol intake, lose weight
Indications for offering urate lowering therapy
Indications for urate-lowering therapy (ULT):
Offer urate-lowering therapy to all patients after their first attack of gout
ULT is particularly recommended if: >= 2 attacks in 12 months tophi renal disease uric acid renal stones prophylaxis if on cytotoxics or diuretics
Pseudogout / calcium pyrophosphate deposition disease (CPPD)
a crystalline inflammatory arthritis caused by the deposition of calcium pyrophosphate crystals intro articular & periarticular tissues
common in elderly people aged >60 yrs
Causes of pseudogout in younger people
in people <60y/o
precipitating factors include haemochromatosis, hyperparathyroidism, ↓Mg2+, ↓Phosphate, acromegaly, Wilson’s disease
Presentation of pseudogout
often asymptotic
acute monoarticular/oligoarticular arthritis most often affecting the knees
other joints include wrists, shoulders, ankles, hands, feet
usually older than gout but also painful, swollen, erythematous joints
NB may present as a sudden worsening of osteoarthritis
Investigations for pseudogout
synovial fluid analysis (positively bifringent rhomboid shaped crystals under polarised light)
serum Ca/PTH (normal or ↑)
USS
X-ray (chonedrocalcinosis i.e. joint carriage calcificatioN)
Synovial fluid analysis results for pseudogout
positively bifringent rhomboid shaped crystals under polarised light
Management of pseudogout
1st line: NSAIDs
2nd line: intrarticular steroids
3rd line: systemic steroids / colchicine
NB colchicine used if NSAIDS/Steroid contraindicated
Systemic lupus erythematous (SLE)
chronic multisystem autoimmune disease of unknown cause, Type II hypersensitivity reaction
most common in women of childbearing age
onset usually age 20-40 yrs
more common in afro-caribbeans/asians
associated with HLA-B8/DR2/DR3
Presentation of Systemic lupus erythematous (SLE)
malar (butterfly) rash (over cheeks & bridge of nose)
fever, fatigue, weight loss
arthritis in 90% of cases (mainly PIP/MCP joints, generally symmetrical)
Rayanuds
photosensitive rash (rash after sun exposure)
discoid lupus (discoid rash in sun exposed area, scaly erythematous plaques)
mouth ulcers
non-scarring alopecia
myalgia
Systemic features of Systemic lupus erythematous (SLE)
Cardiac:
pericarditis (most common), endocarditis (Libman-Sacks endocarditis), CAD, aortic valve disease
Pulmonary:
pleurisy, pulmonary fibrosis, interstitial lung disease)
nephritis:
Most dangerous organ complication and a common cause of death in SLE, affects >30% of SLE pts
depression/anxiety
vasculitis
Investigations for Systemic lupus erythematous (SLE)
Anti nuclear (ANA) antibody (+ve)
Rheumatoid factor (usually -ve)
anti-dsDNA (+ve)
anti-smith antibodies (+ve)
ESR (↑)
FBC (normochromic normocytic anaemia)
CRP (normal)
antiphospholipid antibodies (may be +ve)
Antibodies for Systemic lupus erythematous (SLE)
Anti nuclear (ANA) antibody (+ve)
Rheumatoid factor (usually -ve)
anti-dsDNA (+ve)
anti-smith antibodies (+ve)
NB anti-dsDNA & anti-smith antibodies =most specific
Management of Systemic lupus erythematous (SLE)
Simple analgesia & NSAIDs (use with care due to GI/cardiac/renal risks) for pain control
avoid sun exposure
corticosteroids (usually as induction therapy)
1st line: Hydroxychloroquine
2nd line: add methotrexate or azathioprine
Cyclophosphamide (for life threatening disease e..g nephritis)
Exacerbating factors for Systemic lupus erythematous (SLE)
oestrogen hormones can exacerbate SLE
consider hormonal contraception carefully
Associated conditions for Systemic lupus erythematous (SLE)
antiphospholipid syndrome
Drug induced lupus
95% of cases are positive for anti-histone antibodies
implicated drugs include chlorpromazine, methyldopa, hydralazine, isoniazid, d-penicillamine and minocycline
Systemic sclerosis/scleroderma
auto-immune mediated tissue disease characterised by production of auto-antibodies and overproduction of collagen due to ↑fibroblast activity leading to abnormal connective tissue growth & fibrosis of skin/organs & vasculopathy
Types of systemic sclerosis
limited cutaneous systemic sclerosis (lcSSc):
more common mainly affects distal limbs & face
may present with CREST syndrome (Calcinosis, Raynaud’s phenomenon, oEsophageal dysmotility, Sclerodactyly, Telangiectasia)
associated with anti-centromere antibodies
diffuse cutaneous systemic sclerosis (dcSSc):
less common, affects proximal limbs & trunk as well as face & distal limbs
↑ risk of mortality (mainly pulmonary involvement)
associated with anti-scl-70 antibodies / anti topoisomerase
Scleroderma:
no internal organ involvement, tightening & fibrosis of skin only
Epidemiology of systemic sclerosis
5:1 female:male ratio
presentation usually 30-50 yrs
Presentation of limited cutaneous systemic sclerosis
a subtype is CREST syndrome
- Calcinosis
- Raynaud’s phenomenon
- oEsophageal dysmotility
- Sclerodactyly
- Telangiectasia
scleroderma affects face and distal limbs predominately
Presentation of systemic sclerosis
thickening & hardening of skin (skin appears smooth/shiny/puffy)
sclerodactyly (fibrotic thickening & tightening of skin of fingers & hands)
Raynauds
multiple painful ischaemic digital ulcers
joint stiffness & pain
mask like facies
microstomia
salt & pepper appearance of skin (dyspigmentation)
myalgia
Antibodies for systemic sclerosis
Anti-nuclear (ANA) antibody (+ve)
anti-scl-70 antibodies / anti topoisomerase associated with diffuse cutaneous systemic sclerosis
anti-centromere antibodies associated with limited cutaneous systemic sclerosis
Myositis
systemic inflammatory muscle wasting disease characterised by weakness due to chronic inflammation of skeletal muscle
PM & DM = 2x more common in women
Types of myositis
Polymyositis (PM):
inflammatory myopathy affecting proximal skeletal muscle
Dermatomyositis (DM):
similar to polymyositis but with skin involvement
Inclusion body myositis (IBM):
inflammatory myositis affecting proximal & distal skeletal muscle
Polymyositis
usually presents age 30-60
symmetrical proximal muscle weakness e..g of pelvic & shoulder girdle, dysphagia, muscle tenderness
Dermatomyositis
2 peaks: 5-15yrs & 40-60yrs
symmetrical proximal muscle weakness e..g of pelvic & shoulder girdle, dysphagia, muscle tenderness
gottrons papules (prominent erythematous papules)
heliotrope rash (erythematous rash on upper eyelids)
mechanics hands (hyperpigmentation & thickening of skin on hands)
photosensitive poikiloderma
V-sign erythema (upper chest & neck)
Inclusion body myositis
usually presents >60y/o
slowly progressive (over years), weakness of proximal & distal muscles
Investigating myositis
often a clinical diagnosis
CK (↑) ESR/CRP (↑) LDH (↑) adolase (↑) muscle biopsy (gold standard) EMG ANA (+ve) myositis specific antibodies
Management of myositis
corticosteroids e.g. prednisolone
UV light protection for DM
physiotherapy
Osteoarthritis (OA)
disabling join disease characterised by a non-inflammatory degeneration of the joint complex (articular cartilage, subchondral bone, synovium)
one of the most common chronic diseases
generally age related, ↑ incidence with age
more common in females
Osteoarthritis (OA) risk factors
obesity family history female sex ↑ age history of joint injury/trauma
Osteoarthritis (OA) risk factors
obesity family history female sex ↑ age history of joint injury/trauma mechanical loading/recreational stress on joint physically demanding occupation/sports
Osteoarthritis (OA) presentation
generally affects hips, knees, CMC, DIP, PIP joints & spine
pain (usually associated with activity, relieved by rest, pain at rest is unusual) generally unilateral joint stiffness ↓ROM joint swelling crepitus morning stiffness (<30min)
usually asymmetrical joint involvement
NB in hands Painless nodes (bony swellings): Heberden’s nodes at the DIPJs Bouchard’s Nodes at the PIPJs. Squaring of the thumbs: Deformity of the CMC joint = fixed adduction of the thumb.
Osteoarthritis (OA) investigations
X-ray (loss of joint space, subchondral sclerosis, subchondral cysts, osteophytes of joint margins)
Osteoarthritis (OA) X-ray findings
loss of joint space
subchondral sclerosis
subchondral cysts
osteophytes of joint margins
Osteoarthritis (OA) investigations
X-ray (loss of joint space, subchondral sclerosis, subchondral cysts, osteophytes of joint margins)
synovial fluid analysis (non inflammatory, yellow/clear, normal WCC)
Osteoarthritis (OA) management
General:
weight loss
physio
Symptomatic:
1st line: paracetamol & topical NSAIDs
2nd line: COX-2 inhibtors, oral NSAIDs, intra-articular steroids
Surgical:
joint replacement
Reactive arthritis
an inflammatory arthritis that occurs after expiosure to certain gastrointestinal & genitourinary infections, its a type of seronegative spondyloarthritis
strong association with HLA-B27
usually seen in young adults especially men after STI
Used to be know as Reiters syndrome
Causes of reactive arthritis
Post enteric: Campylobacter*, salmonella, shigella
Post-venereal: chlamydia trachomatis*
Presentation of reactive arthritis
usually presents 2-4 weeks post infection
classic triad:
- urethritis (can’t pee)
- conjunctivitis (can’t see)
- arthritis (can’t climb trees)
acute onset nausea, fatigue, fever, diarrhoea, urogenital symptoms (dysuria, pelvic pain)
asymmetrical predominantly lower extremity oligoarthritis lower back pain common
Investigations for reactive arthritis
ESR/CRP (↑) Anti nuclear (ANA) antibody (-ve) Rheumatoid factor (-ve) test for HLA-B27 (often +ve) synovial fluid analysis (↑WCC) stool/urogenital/throat cultures X-rays (normal)
Management of reactive arthritis
Symptomatic:
NSAIDs & intraarticular steroids
treat cause:
Abx (to treat organism identified)
persistent disease:
sulfalazine / methotrexate
Septic arthritis
infection producing inflammation in a native or prosthetic joint, most commonly due to haematogenous spread of infection
Septic arthritis aetiology
stap aureus = most common overall
in young sexual active adults Neisseria gonorrhoea is the most common cause
Risk factors for Septic arthritis
↑ age diabetes prosthetic joint immunosuppression underlying joint disease e.g. RA
Presentation of Septic arthritis
knee = most commonly affected joint in adults knee/hip/ankle = most commonly affected joint in children
acute onset of fever, joint pain, restricted ROM
monarticular swollen, erythematous, warm, tender joint
Investigating Septic arthritis
synovial fluid sampling* (↑ WCC, positive culture, yellowish/green colour, turbid)
CRP/ESR (↑)
FBC (↑ WCC)
USS (effusion)
blood cultures
X-ray (unremarkable)
Management of Septic arthritis
IV Abx:
e.g. flucloxacillin (clindamycin/erythromycin if penicillin allergy)
give for 6-12 weeks
joint drainage & aspiration
arthroscopic lavage
Prosthetic joint septic arthritis
often due to skin pathogens eg. staph epidermis or staph aureus if early, i.e. within 12 weeks of implantation
later onset usually doe to haematogenous spread e.g. E. coli, staph aureus, pseudomonas aeruginosa
often managed surgically with irrigation & debridement or exchange of arthroplasty
Synovial fluid analysis in septic arthritis
↑ WCC
positive culture
yellowish/green colour
turbid
Paget’s disease
slowly progressive disease of ↑ bone turnover causing lamellar bone to be replaced with woven bone, due to disorder of osteoclasts with ↑ osteoclastic bone resorption
onset usually age >55, slight male predominance
Risk factors for Paget’s disease
Family history of pagets
male gender
↑ age
Presentation of Paget’s disease
commonly asymptomatic (only ~5% of pts symptomatic)
bone pain e.g. pelvis/lumbar spine/femur
if untreated leads to bossing of skull, bowed tibia
pathological fractures
↑ skin temp in areas of disease
usually only affects 1 bone
impaired hearing (due to cranial nerve entrapment)
Investigations for Paget’s disease
PTH/phosphate/calcium (normal)
ALP - Alkaline phosphatase (↑↑↑)
X-ray (advancing V-shaped lytic lesions, pathological fractures, cotton wool, osteolysis↑ & bone formation↑)
bone scan (areas of dense uptake in pagetoid bone)
Markers of bone turnover e.g. PINP/CTx/NTx (↑)
Management of Paget’s disease
Symptomatic treatment:
NSAIDs/paracetamol for pain
Vit D & Calcium supplements
1st line: Bisphosphonates e.g. zolendronate
2nd line: Calcitonin
Complications of Paget’s disease
bone sarcoma
high output cardiac failure
Osteoporosis
a complex skeletal disease characterised by low bone density and micro-architectural defects in bone tissue resulting in ↑ bone frailty & ↑ susceptibility to fractures
Osteoporosis
a complex skeletal disease characterised by low bone density and micro-architectural defects in bone tissue resulting in ↑ bone frailty & ↑ susceptibility to fractures
more common in women
age of onset usually 50-70yrs
very common overall (1/3 women & 1/5 men in their lifetime)
T-score
based on bone mass of young reference population
Z-score
bone mass adjusted for age, gender, ethnicity
Bone density measurements
normal:
T-score ≥-1
Osteopenia:
T-score -2.5
Osteoporosis:
T-score ≤-2.5
Severe Osteoporosis:
T-score ≤-2.5 + a fracture
Risk factors for osteoporosis
female sex ↑ age white ethnicity psot menopausal corticosteroid use smoking low BMI family history excessive alcohol intake Chronic disease (CKD, RA, UC, Crohns, coeliac, cushing etc) drugs (e.g. PPIs, anticonvulsants)
Investigating osteoporosis
DEXA scan (T-score ≤-2.5)
Fracture risk assessment tool (FRAX) / QFracture (to asses 10 year risk of frailty fracture)
investigate for underlying cause
Management of osteoporosis
For everyone: Vit D supplementation ± calcium supplementation (depending on dietary intake)
1st line: bisphosphonates e.g. alendronate (1st line) or risendronate
2nd line: denosumab (if bisphosphonates contraindicated / special instructions can’t be adhered to)
3rd line: Raloxifene or Strontium ranelate
Bisphophonates
Bisphosphonates are analogues of pyrophosphate, they inhibit osteoclasts by reducing recruitment and promoting apoptosis.
Examples:
alendronate, risendronate
Side effects:
oesophagitis/oesophageal ulcers
osteonecrosis of the jaw
How to take:
Tablets should be swallowed whole with plenty of water while sitting or standing; to be given on an empty stomach at least 30 minutes before breakfast (or another oral medication); patient should stand or sit upright for at least 30 minutes after taking tablet’
Hypocalcemia/vitamin D deficiency should be corrected before giving bisphosphonates.
Contraindications include inability to follow special instructions for administration & history of peptic ulcers
Stopping Bisphophonates
The duration of bisphosphonate treatment varies according to the level of risk. Some authorities recommend stopping bisphosphonates at 5 years if the following apply:
patient is < 75-years-old
femoral neck T-score of > -2.5
low risk according to FRAX/NOGG
Osteomalacia
is a metabolic bone disease characterised by incomplete mineralisation of the underlying mature bone matrix following growth plate closure in adults
the primary cause is Vit D deficiency
NB if its before growth plate closure = rickets
Risk factors for osteomalacia
dark skin ↑ age obesity pregnancy housebound/institutionalised liver disease e..g cirrhosis CKD limited sun exposure anticonvulsant therapy malabsorption syndromes diet (e.g. vegan)
Presentation of osteomalacia
bone pain & tenderness
pathological fractures
waddling gait & difficulty walking
muscle weakness/spasms/cramps
NB in rickets: knock knees, bow legs, features of hypocalcaemia
Investigations for osteomalacia
serum 25-hydrovitamin D (↓) Ca2+ (↓/normal) Phosphate (↓) urea & creatinine (↑ ratio) alkaline phosphatase (↑) 24h urine calcium (↓) PTH (↑)
X-rays (translucent bands/↓ bone mineral density, pseudo fracture - linear areas of low bone density sourounded by sclerotic borders)
DEXA scan (↓ bone density)
Management of osteomalacia
dietary advice
Vit D & calcium supplementation (nb high dose for 8-12 weeks to replenish stores, then lower dose as maintenance)
Osteomyelitis
an infection of the bone marrow which may spread to the bone cortex & periosteum via haversian canals, generally involving a single bone
Types of Osteomyelitis
Haematogenous:
due to haematological bacterial seeding from a remote site, usually monomicrobial
more common in children & adolescents
Direct (contiguous):
direct contact of infected tissue with bone, usually more localised clinical signs
more common in adults
Aetiology of Osteomyelitis
staph aureus most common
in sickle cell pt most common = salmonella
Presentation of Osteomyelitis
limp reluctance to weight bear non specific pain at site of infection malaise, fatigue, fever local inflammation, tenderness, erythema, swelling
vertebral involvement very common in adults
Investigating Osteomyelitis
may be a clinical diagnosis
CRP/ESR (↑) FBC (↑WCC) blod cultures X-ray of affected area MRI* (Imaging modality of choice)
Management of Osteomyelitis
Abx
e.g. flucloxacillin (or erythromycin/clarithromycin if penicillin allergy)
surgical:
bone debridement, abscess drainage, remove infected prosthesis
Risk factors for Osteomyelitis
trauma prosthetic orthopaedic device diabetes PAD IVDU alcoholism immunosuppression
Compartment syndrome
a condition of ↑ pressure within a muscular compartment leading to impaired tissue perfusion due to the ↑ pressure in a closed anatomical space compromising circulation and leading to temporary/permanent muscle & nerve injury
Types of Compartment syndrome
acute:
usually due to trauma, requires prompt diagnosis & treatment
chronic:
usually caused by exercise, present wit recurrent pains & disability which subsides when exercise is stopped
Sites for Compartment syndrome
upper & lower limb compartments
most commonly anterior & deep posterior compartment of leg & the solar compartment of the forearm
i.e. supracondylar fractures and tibial shaft injuries
Aetiology of Compartment syndrome
Acute:
trauma, burns, casts/constrictive bandages, fractures, haematomas
Chronic:
usually in lower legs, exercise induced
Presentation of Compartment syndrome
pain, pallor, paraesthesia, pulselessness, paralysis, poikilothermia
soft tissue sweeling
cold peripheries
abesnt/weak pulses
pain (often out of proportion of extent of injury
Investigating Compartment syndrome
usually clinical diagnosis
compartment pressure measurement (↑, <40mmHg)
Management for Compartment syndrome
prompt & extensive fasciotomy (surgical emergency)
in burns escharotomy
IV fluid resuscitation (to prevent renal failure from myoglobinuria)
if muscle is necrosed may need debridement or amputation
Developmental dysplasia of the hip (DDH)
refers to hip instability, subluxation/dislocation of the femoral head and/or acetabular dysplasia in the developing hip joint
~20% are bilateral
~80% of all cases are female
Risk factors for Developmental dysplasia of the hip (DDH)
female sex breech presentation family history of DDH first born child oligohydramnios multiple pregnacy
Routine screening for Developmental dysplasia of the hip (DDH)
routine part of NIPE & new-born examination at 6-8 weeks
Barlow test: attempts to dislocate articulated femoral head
Ortolani test: attempts to relocated dislocated femoral head
also look at leg length symmetry, asymmetrical gluteal/thigh folds, Galeazi sign (level of knees with hips & knees flexed)
Presentation of Developmental dysplasia of the hip (DDH)
generally asymptomatic in early life
later:
hip pain abnormal leg positing
delayed crawling/walking
toe walking
Investigating Developmental dysplasia of the hip (DDH)
USS (subluxation on provocation test, abnormal relationship between femoral head & acetabulum)
X-ray (abnormal relationship of femoral head & acetabulum)
NB use X-ray first line if infant >4.5 months