Week 11 Flashcards
Describe tendinopathy
chronic tendon injury of over use - repetitive loading
degeneration, disorganisation of collagen fibres
increased cellularity
little inflammation
loss of balance between micro damage from overuse and reparative mechanisms
What are the risk factors for tendinopathy?
age chronic disease diabetes rheumatoid arthritis adverse biomechanics repetitive exercise recent increase in activity quinolone antibiotics
Describe the pathology of tendinopathy
deranged collagen fibres/regeneration with a scarcity of inflammatory cells
increased vascularity around the tendon
failed healing response to micro tears
inflammatory mediators release IL-1, NO, PG’s cause apoptosis, pain and provoke degeneration through release of MMPS
What are common tendinopathies?
achilles rotator cuff tennis elbow (lateral epicondylitis golfers elbow (medial epicondylitis) patella hamstring adductor plantar fasciitis
What are the clinical features of tendinopathy?
pain swelling thickening tenderness provocation tests
How is tendinopathy diagnosed?
clinical history
ultrasound
MRI - best seen on T1
What are the non operative treatments of tendonopathy?
NSAIDs activity modification physiotherapy GTN patches PRP injection prolotherapy extracorporeal shockwave therapy topaz - radiofrequeny collation steroid injection
Describe physiotherapy in the treatment of tendonopathy
eccentric loading
contraction of the musculotendinous unit whilst it elongates
Describe operative treatment of tendonopathies
debridement
excision of diseased tissue
possible to deride 50% of tendon without loss of function
Describe compartment syndrome
elevated interstitial pressure within a closed fascial compartment resulting in microvascular compromise
common sites - leg, forearm, thigh
What are the causes of compartment syndrome?
increased internal pressure - bleeding, swelling, iatrogenic inflammation
increased external compression - casts, bandages, full thickness burns
combinations
Describe the pathophysiology of compartment syndrome
decreased perfusion muscle ischaemia muscle swelling increased permeability - fluid leaks into interstitial space increased pressure autoregulatory mechanisms overwhelmed muscle necrosis and myoglobin release loss of function, extremity or loss of life
Describe the end stage of compartment syndrome
stiff fibrotic muscle compartments
impaired nerve function
clawing of limbs
loss of function
What are the clinical features of compartment syndrome?
pain - out of proportion to that expected from the injury
pain on passive stretching of the compartment
pallor
parathesia
paralysis
pulselessness
How is compartment syndrome diagnosed?
site swelling shiny ski autonomic responses - sweating, tachycarida pulses present until late stages deep nerves affected first - 1st dorsal web space - deep perineal nerve normal pressure 0-4mmHg DBP-CP <30mmHg CP>30mmHg
What is the treatment of compartment syndrome?
open any constricting dressings / bandages reassess surgical release later wound closure skin grafting / plastic surgery input
Describe surgical release in compartment syndrome
full length decompression of all compartments
excise any dead muscle
leave wounds open
repeat debridement until pressure dow and all dead muscle excised
Describe the preoperative care in compartment syndrome
adequate hydration fluid loss monitor and regulate electrolyes correct acidosis myoglobinuria renal function
Describe the treatment in late presentation of compartment syndrome
irreversible damage already present
fasciotomy will predispose to infection
consider non-operative treatment
splint in position of function
What is vasculitis?
inflammation of the blood vessels
What are the main secondary causes of vasculitis?
infection
underlying disease - cancer, autoimmune diseases such as RA, SLE or IBD
cold injury
drugs
What are the main infectious causes of vasculitis?
meningococcal septicaemia
streptococcus
Describe cryoglobulinaemia
cold causes antibodies to acitivate
these antibodies attack, clump and destroy red blood cells
this blocks and irritates the vessels
peripheral are worst affected
What drugs can cause vascultits?
anti thyroid drugs (carbimazole) micocyclin hydralazine penicillamine antibiotics anticonvulsants
What are the general features for all primaries vasculitis?
systemic inflammation -fever, malaise, weight loss, myalgia, arthralgia, night weats
What does large vessel vasculitis cause?
end organ ischaemia or infarction
What does medium vessel vasculitis cause?
localised ischaemia or infarction
What does small vessel vasculitis cause?
organ specific inflammation
What are the 2 main types of large vessel vasculitis?
giant cell (common) takayasu (rare)
What are 2 types of medium vessel vasculitis?
polyarteritits nodosa (PAN) Kawasaki disease (children only)
What are the 2 types of small vessel vasculitis?
immune complex mediated vasculitis
ANCA associated vasculits
What types of immune complex mediated vasculitis are there?
HSP
cryoglobulinaemia
What are the ANCA associated vasculitis?
microscopic polyangitis
granulomatosis with polyangitis (Wegener’s)
eosinophilic granulomatosis with polyangitis (churn-strauss disease)
Describe giant cell arteritis
elderly
common
women
What re the clinical features of giant cell arteritis?
fatigue headaches jaw claudication scalp tenderness test - very high ESR definitive test - biopsy
What is the sudden blindness associated with giant cell arteritis called?
amaurosis fugax
Describe polymyalgia rheumatica
considered related disorder to giant cell
elderly, mainly women
pain is the main symptom
pain and stiffness in muscles of neck, shoulder and pelvis
not particularly weak
high ESR
better with steroids
Describe takayasu’s arteritis
pulseless disease or aortic arch syndrome
very rare
younger women (15-25)
systemic features come early and may resolve by diagnosis
late features of vascular insufficiency in aorta and large tributaries
- bruits, absent or reduced pulses
claudication - arms, legs, spine, gut
ischameic heart disease, heart failure, pulmonary hypertension
headaches and amaurosis fugax
BP variability - syncope, hypertension, variable BP between limbs
diagnosis - imaging, angiography, CT
Describe polyarteritis nodosa
medium vessel
fever and weight loss
malaise and myalgia
organs generally - infarction or ischaemia - gut,
brain
angina
liver
skin - gangrene, purpura, nodules
peripheral nervous system - pain in distribution of nerve, loss of sensory/motor
limbs - claudication
kidney - infarction, renal artery stenosis, renal aneurysms, hypertension
Describe kawasaki disease
only in children
aneurysm found in medium to large sized arteries
coronary arteries - MI
axillary, iliac and popliteal arteries
early features - high fever, miserable, mucositis, conjunctivitis
Describe HSP
commonest vasculitis in childhood less common in adults possible infective tirgger palpable purpura (extensor surfaces, starts peripherally) abdominal pain arthritis complicated by - renal involvement, intersucception / infarction pain misery testis pain/infarction
What does ANCA stand for?
anti-neutrophil cytoplasmic Ab
What are the 2 types of ANCA?
cytoplasmic c-ANCA
perinuclear p-ANCA
When is cANCA positive?
very specific for granulomatous polyangitis (Wegener’s )
when is pANCA and MPO positive?
microscopic polyangitis
crescentic glomerulonephritis
eosinophilic granulomatous polyangitis
When is pANCA positive and MPO negative?
IBD
RA
sclerosing cholangitis
Describe granulomatous polyangitis
Wegener’s
classically involves URT, LRT and kidneys
Describe eosinophilic angitis
churg strauss asthma eosinophilic infiltrates eosninophilia eosinophil rich granulomata peripheral neuropathy
Describe microscopic polyangitis
small and medium sized vessels chronic inflammation 5 most common clinical manifestations of MPA are kidney glomerulonephritis weight loss skin lesions peripheral neuropathy, mononeuritis multiplex fevere no granuloma pANCA 75%
What is the treatment of primary vasculitis?
corticosteroids
other immune suppression
What is the commonest cause of vasculitis in children?
henoch scholein purpura
What are 3 ANCA associated vasculitis?
microscopic polyangitis
granulomatosis with polyangitis
eosinophilic grnulomatosis with polyangitis
Describe septic arthritis
pain, fever, swollen joint, loss of function
staph.aureas, neisseria gonorrhoea, haemophilus influenza (children)
increased risk if steroids, RA
suspected septic arthritis is a medical emergency
How can bacteria infect a joint space?
hematogenous
dissemination from osteomyelitis
spread from adjacent soft tissue infection
medical procedures
penetrating damage by puncture or traumaa
What investigations should be carried out for septic arthritis?
joint aspirate - microbiology from gram stain and culture
blood culture
FBC -leukocytosis
xray - no value
What affect can septic arthritis have in the joint if it is not treated?
synovial inflamed with fibrin exudation and numerous neutrophil polymorphs
loss of articular cartilage may lead to secondary osteoarthritis
What are other types of septic arthritis?
lyme disease - borrelia burgdoferi
brucellosis
syphilitic arthritis - congenital and acquired
What types of crystal arthropathy are there?
gout and pseudogout
Describe gout
excess levels of uric acid - leads to deposition of urate crystals in joints or soft tissue (top)
acute - precipitation in joint stimulates acute inflammatory process
chronic gout - top formation
how is gout diagnosed?
aspirate - negatively befringement needle shaped crystals on polarised microscopy
serum urate levels and U&Es
What can cause primary gout?
hyperurciaemia due to genetic predisposition – Lesch Nyhan syndrome
What can cause secondary gout?
myeloproliferative disorder
leukaemia treated with chemo
thiazides
chronic renal disease
What tend to raise uric acid levels?
increasing age obesity high alcohol intake high protein diet diabetes mellitis
What is the management of gout?
NSAIDs
alternatives - colchicine, corticosteroids
if repeated - allopurinol - xanthine oxidase inhibitor
uricosuric agent (probenecid) increased secretion of uric acid in the urine
Describe pseudogout
calcium pyrophosphate crystal deposition
synovial
cartilage and extra-articular tissues (chondorcalcinosis)
acute or chronic
primary or secondary (hyperparathyroidism, haemochromatosis)
positively befringement rhomboid shaped crystals on aaspiration
What is the management of pseudo gout?
aspiration helps to reduce pain and swelling
NSAIDs
colchicine
Describe reactive arthritis
sterile synovitis which occurs following an infection
What are the common trigger organisms for reactive arthritis?
salmonella, shigella, yersinia, chlamydia thachomatis
What are the clinical features of reactive arthritis?
acute, asymmetrical lower limbs arthritis
more common in men
days-weeks post infection
also - enthesitis (plantar fasciitis), sacroiliitis, spondylitis anterior uveitis, conjungtivism keratoderma blenorrhagia
What is the management of reactive arthritis?
little evidence of treating the triggering infection alters the course of the disease
pain control - NSAIDs, intra-articular steroids
Describe enteropathic arthritis
form of reactive synovitis seen in association with UC and crohns disease
an asymmetrical lower limb arthritis
treatment of bowel disease and NSAIDs
Describe osteoarthritis
degenerative joint disease commonest form of arthritis middle aged / elderly weight bearing joints - hip, knee pathology - disorder of articular cartilage
What can cause secondary osteoarthritis?
fracture previous sepsis RA osteonecrosis gout haemochromatosis ochronosis peripheral neuropathy
What can be seen on xray of an osteoarthritic joint?
narrowed joint space loss of cartilage
bony spurs
Describe the pathophysiology of OA
loss of articular cartilage, exposure of underlying bone subchondral cysts and sclerosis, osteophytes
synovium becomes hyper plastic, mild inflammation, bony detritus
What is the most common primary bone tumour?
myeloma
Which cancers most commonly metastasise to bone?
bronchus, breast, prostate, kidney, thyroid (follicular)
Which childhood cancers often metastasise to bone?
neuroblastoma
rhabdomyosarcoma
What are the effects of metastases to bone?
often asymptomatic bone pain bone destruction long bones - pathological fractures spinal metastases- vertebral collapse, spinal cord compression, nerve root compression, back pain hypercalcaemia
What is the most common type of bone metastasis?
lytic
How is the bone destroyed in lytic tumours?
osteoclasts, not tumour cells
stimulated by cytokines from tumour cells
inhibit by biphosphonates
How are sclerotic bone metastases formed?
reactive - osteoblasts induced by tumour cells
Which cancers sometimes lead to solitary bone metastases?
renal and thyroid
often long survival
surgical removal often valuable
Describe myeloma
commonest malignant primary bone tumour
monoclonal proliferation of plasma cells
solitary (plasmacytoma) or multiple myeloma
orthopaedic and medical consequences
Describe the clinical effects of myeloma
bone lesions - punched out lytic foci, generalised osteopenia
marrow replacement - anaemia, infections
immunoglobulin excess - ESr > 100
serum electrophoresis - monoclonal band
urine - immunoglobulin chains (bence jones protein)
Name 3 benign primary bone tumours
osteoid osteoma
chondroma
giant cell tumour
name 3 malignant primary bone tumours
osteosarcoma
chondrosarcoma
ewing’s tumour
Describe osteoid osteoma
a small, benign osteoblastic proliferation
common any age, especially male adoslescents
any bone - especially long bones and spine
pain worse at night, relieved by aspirin, scoliosis
junta-articular tumours - sympathetic synovitis
Describe osteosrcoma
a malignant tumours whose cells form osteoid or bone peak 10-25 metaphysics of long bones mainly around knee male predominance early lung metastases
Describe paget’s disease
common in elderly anglo-saxon origin excessive bone turnover increased osteoclasts, increased bone formation, structurally weak bone disorganised architecture vertebrae, pelvis, skull, femur
What are the results of paget’s disease?
bone pain deformity pathological fracture osteoarthritis deafness spinal cord compression high cardiac output- HF paget's sarcoma
Describe paget’s sarcoma
second osteosarcoma peak in elderly usually lytic long bones >spine very poor prognosis early metastases to lung and bone
Describe enchondroma
lobulated mass of cartilage within medulla
common
any age
>50% hands and feet, long bones
often asymptomatic in long bones
hands - swelling
low cellularity, often surrounded by plates of lamellar bone
Describe osteocartilaginous exostosis
bengin outgrowth of cartilage with endochondral ossification
probably derived from growth plate
very common- usually in adolescent
metaphysis of long bones - not craniofacial
What is the genetic condition associated with oesteocartilaginous exostosis?
multiple diaphyseal aclasis
autosomal dominant
Describe chondrosarcoma
primary or from pre-exisitng enchondroma or exostosis
central, within medullary cavity or peripheral on bone surface
predominantly middle aged and elderly
more males
axial skeleton, pelvis, ribs , shoulder girdle, proximal femur, humerus.
rare in hands or feet
Describe Ewing’s sarcoma
peak 5-15 years long bones flat bones of limb girdles early metastases to lung, marrow and bone (22:11) balanced translocation
Name 2 types of autoimmune myositis
polymyositis
dermatomyositis
Describe polymyositis
chronic inflammation of striated muscle
Describe dermatomyositis
chronic inflammation of striated muscle with a rash
elderly - associated with malignancy
children - not malignant
What are the diagnostic features of polymyositis and dermatomyositis?
painful proximal myopathy with weakness evidence of inflammation in muscle - biopsy, MRI elevation of muscle enzymes characteristic EMG patten characteristic JDM rash
Describe the rash in dermatomyositis
heliotrope rash - purple hue on eyelids butterfly distribution vasodilated capillaries gottron's papuls nailfold features
what are the investigations in JDMS?
muscle enzymes - CK, ALT, LDH
MRI
muscle biopsy
clinical monitoring - FVC, power testin
Describe the systemic involvement in lupus
dermatitis renal liver spleen lymph nodes CNS systemic vasculitis serositis - pleurisy, pericarditis, peritonitis arthritis failure to thrive
What is included the the diagnosis criteria for SLE?
malar rash discoid rash photosenstiivty oral ulcers arthrits serositis renal disorder neurological disorder haematolgical disorder immunological dirorder ANA
Describe ANA testing for lupus
sensitive but not specific
many causes of positive ANA including; other AI conditions, drug induced, hepatic disease, pulmonary disease, malignant etc
Descrbir anti-dsDNA
specific but not sensitive
Describe the investigation of SLE
FBC renal Ix acute phase response ANA dsDNA Ro/La low complement excess total immunoglobulins
What organs can systemic scleroderma affect?
lung
renal
GIT
joints
How can inflammation be controlled in connective tissue disease?
steroids
DMARDS
biologics
In what ways are steroids excellent immunosuppressants?
rapid onset
easy to administer
able to treat wide variety of inflammatory conditions
Why are steroid sparing agents used?
steroids cause - weight gain and fluid retention glaucoma osteoporosis infection hypertension hypokalaemia peptic ulceration and GI bleed psychological and psychiatric symptoms
Which immunosuppressants are inhibits of DNA synthesis?
methotrexate
azithioprine
mycophenolate
which immunosuppressant drugs are lymphocyte signalling inhibitors?
cyclosporin
tacrolimus
sirolimus
leflunomide
What are the adverse effects of methotrexate?
GI -nausea, vomiting, diarrhoea, hepatitis, stomatitis
haematological - leukopenia
others - frequent infections, pulmonary fibrosis
Describe methotrexate in practise
mostly used for RA and psoriatic arthritis
steroid sparing agent in giant cell arteritis
given once a week with folic acid 4 days later
normally orally
takes weeks to work
blood monitoring
How does azathioprine work?
converted within cells into a nucleoside analog
incorporated into DNA and RNA chains leading to termination of nucleic acid strands
cell growth and metabolism halts
preferential action of lymphocytes as other cells have purine salvage pathway
Which enzyme must be checked before starting azathioprine?
TPMT
Describe azathioprine in practise
mostly used for IBD and Myasthenia gravis, eczema orally on a daily basis takes several weeks to work monthly bloods
How does cyclosporin work?
small molecule inhibitor of calcineurin
effect of inhibiting signal transduction from the activated TCR complex
profound inhibition of T cell activation
What are the adverse effects of cyclosporin?
nephrotoxicity hypertension hepatotoxicity anorexia and lethargy hirsutism paraesthesia does not suppress bone marrow
Describe tacrolimus
different class of drug but similar mechanism of action as cyclosporin
more potent activity
very similar use to cyclosporin but may be better tolerated
What is cyclosporin used for?
organ transplantation or some inflammatory conditions orally daily therapeutic drug monitoring P450 enzymes blood tests regularly
What are the disadvantages of immunosuppressants?
often insufficient to control inflammatory disease with subsequent progression slow onset significant toxicities bone marrow suppresison frequent infections
Describe biologic therapies
able to target specifically designated components of the immune systems
able to do so with minimal off target effects
usually parenteral route
relatively favourable side effect profile
What are the side effects of biologic therapy?
hypersensitivity reactions
infusion reactions
mild GI toxicity
What infection is more likely with anti-TNF therapy?
TB
particularly disseminated TB
also salmonella and listeria
What infection is more likely with rituximab?
generalised risk of serious infection
high risk of hep B reactivation
What infections are more likely with abatacept?
pneumonia and respiratory tract infections
What infections are more likely with anti IL-1 therapy?
RTIs and pneumonia
Describe the burdens of back pain
financial - work, expenses insomnia emotional stress relationship breakdowns severe emotional distress for partners limitations in fulfilling family tasks
What are the 3 broad categories of back pain?
mechanical - non specific low back pain
systemic
referred
Describe mechanical back pain
onset at any age, variable rate
generally worsens with movement or prolonged standing
better at rests
early morning stiffness <30 minutes
What are the causes of mechanical back pain?
lumbar strain/sprain
degenerative discs / facet joints
disc prolapsed, spinal stenosis
compression fractures
Describe degenerative disc disease
spondylosis
many asymptomatic
increase with flexion, sitting, sneezing
Describe degenerative facet joint disease
more localised
increased with extension
Describe the management of non-specific LBP
keep diagnosis under review reassurance - careful with terminology education, promote self management advise to stay active exercise programme and physiotherapy analgesics as appropriate (avoid opiates) also acupuncture avoid infections, traction, lumbar supports
Describe raduculopathy
disc prolapse herniated nucleus pulposis may be acute, increase cough more leg pain than back - sciatica straight leg testing positive reduced reflexes most resolve within 12 weeks wait with investigations - MRI <10% need surgery (helps leg, not back pain)
Describe spinal stenosis
anatomical narrowing of spinal canal congenital and / or degenerative often presents with "claudication" in legs/calves worse walking, rest in flexed position natural history variable investigations xray, MRI surgery generally high risj
Describe cauda equina syndrome
spinal cord ends at L1/2 neuropathic symptoms - bilateral sciatica, saddle anaestehsia bladder or bowel dysfunction reduced anal tone usually large prolapsed disc urgent neurosurgical review
What is spondylolisthesis?
"slip" of one vertebra on the one below mainly asymptomatic pain may radiate to posterior thigh increase with extension rarely needs surgery (if severe)
Describe compression fractures
elderly patient
sudden onset, severe
radiates in “belt” around chest / abdomen
most pain settles in 3 months
associated osteoporosis - risk of recurrence is high
investigations xray, DEXA scan
treatment - conservative, calcitonin, vertebroplasty or kyphoplasty
What can cause referred pain in the back?
aortic aneurysm
acute pancreatitis
peptic ulcer disease
acute pyelonephritis / renal colic
What are the causes of systemic back pain?
infection - discitis, osteomyelitis , epidural abscess
malignancy
inflammatory
Describe infective discitis
fever, weight loss
constant back pain - rest, night pain
immunosuppressed, diabetes, IV drug use
What is the diagnosis / treatment of discitis?
bloods - FBC, ESR, CRP, blood cultures imaging - Xray, MRI radiology guided aspiration most common staph aureas IV antibiotics & surgical debridement look for source
Describe malignancy as a cause of back pain
history of malignancy LP thomas knows best lung, prostate, thyroid, kidney, breast onset >50 constant pain, often worse at night systemic symptoms, primary tumour signs & symptoms Xray, MRI, bone scan look for primary
Describe inflammatory back pain
onset <45 years, often teens early morning stiffness >30 minutes back stiff after rest and improves with movement may wake 2nd half of night family history
Describe the overall approach to back pain
history - red flags
examination - back, neuro, abdomen
most = non specific LBP = no further investigation
keep diagnosis under review - investigate if unusual
imaging - xray, MRI
bloods - if suspect infective / inflammatory / myeloma screen
What are the red flag symptoms of back pain?
new onset <16 or >50 following significant trauma previous malignancy systemic - fevers, malaise, weight loss previous steroid use IV drug abuse, HIV or immunocompromised recent significant infection urinary retention non-mechanical pain (worse at rest "night pain" thoracic spine pain
What are the red flag signs in back pain?
saddle anaesthesia reduced anal tone hip or knee weakness generalised neurological deficit progressive spinal deformity
What are the yellow flags in back pain?
attitudes beliefs compensation diagnosis emotions family work relationship
What are the symptoms of axial spondyloarthritis?
inflammatory back pain fatigue arthritis in other joints inflammation outside joints - uveitis, psoriasis, IBD, other- heart, lungs, osteoporosis family history of above
What gene is thought to be involved in axSpA and AS?
HLA-B27
What is physical activity?
any bodily movement produced by skeletal muscles that requires energy expenditure
includes broad range of activities - everyday activities,
household chores
occupational tasks
leisure time physical activity
exercise
What is FITT?
energy expended frequency intensity time type
What is exercise?
physical exercise that is planned, structures, repetitive and purposeful (aimed at improving or maintaining on or more component of physical fitness)
What is meant by physical fitness?
a set of attributes that people have or achieve that relates to the ability to perform physical activity
What types of physical fitness are there?
cardiorespiratory endurance
muscular strength
balance and coordination
flexibility
Describe traumatic sports injuries
fractures and dislocations
major muscle - ligament-tendon injuries
head and spinal injuries
chest and abdominal injuries
What are the types of fractures?
transverse, oblique, spiral, comminuted, avulsion - a piece of bone attached to tendon or ligament is torn away
What are the clinical features of a fracture?
pain, tenderness, localised bruising, swelling, deformity, restriction of movement
Describe injuries to articular cartilage
associated with soft tissue injuries (ACL rupture)
initial xray often normal - suspect if sprain remains painful and swollen longer than expected
diagnose on MRI
arthroscopy to confirm and remove loose fragments
may predispose to premature osteoarthritis
do not usually heal fully - variety of treatment to improve healing - perforation, alteration of joint loading, cell transplantation
What is dislocation?
trauma produces complete dissociation of the articulating surfaces
What is subluxation?
some contact of articulating surfaces remains
What are the complications of joint dislocations / subluxations?
associated nerve or blood vessel damage
xray to exclude fracture
What is the treatment of joint dislocations / subluxations?
reduction muscle relaxants may be required protect to allow soft tissue to heal early protected mobilisation rebuild muscle strength
Describe strain / tear of muscle
occur when demands exceed muscle capacity
common if cross 2 joints - hamstrings, quadriceps and gastrocnemius
common during sudden acceleration or deceleration
What is the management of strains / tears of muscle?
first aid to minimise bleeding, swelling and inflammation electrotherapy soft tissue therapy stretching strengthening
What are the predisposing factors to muscle tears?
inadequate warm up insufficient joint range of motion excessive muscle tightness fatigue/ overuse / inadequate recovery muscle imbalance previous injury poor technique altered biomechanics
What is the treatment of achilles tenonopathy
active rest
alter training schedule - no hills / decrease pace
heal wedge
NSAID
immobilisation
surgery for chronic tendonitis or rupture
no steroid injections
Give an overview of RA
chronic multisystem disease autoimmune hallmark is synovitis affecting any synovial joint small joint predominance but distal sparing multiple extra-articular manifestations
Describe the aetiology of RA
HLA-DR4 and other genetic factors shared epitope smoking infection (EBV, TB, porphyromonas gigivalis) hormonal
Describe the pathophysiology of RA
synovitis - immune cells invading a normally relatively acellular synovial in the form of a pannus
What is a pannus?
hyperplastic, invasie tissue leading to cartilage breakdown, erosions and consequent reduced function
What are the clinical features of RA?
synovitis
symmetrical
small joints in hands and feet early on : shoulder/hip at onset rare
inflammatory -pain, eryhtema, swelling, EMS
tenosynovitis, bursitis, CTS
constitutional - fatigue, weakness, low grade fever, weight loss, anorexia
What are the classical joint features in late RA?
boutonniere swan neck Z-thumb volar subluxation of wrist ulnar deviation digits radial deviation wrist piano key ulnar head
What systemic effects can RA have?
respiratory cardiac dermatological opthalmic neurological haematological
What investigations should be done for RA?
FBC U&Es LFTs ESR / CRP RF ACPA (ANA)
Describe rheumatoid factor
autoantibody again Fc portion of IgG usually IgM against IgG 60% sensitive, 80% specific other conditions - SLE, SBE, SScl, SjS, TB, EBV, healthy controls etc part of assessment, not diagnostic
Describe anti CCP
sensitive 60%, specific 80-90%
picks up those who may be RF negative
predictor of worse prognosis, more erosions, resistant disease
linked with smoking (increases citrullination)
Describe imagine in RA
Xrays - soft tissue swelling, joint space narrowing, erosions, periarticular OP
USS: more sensitive for synovitis and erosions
MRI -bone marrow oedema
What are the differentials for RA?
OA SLE PMR psoriatic arthropathy sponyloarthropathies reactive arthritis sarcoid CPPD (calcium pyrophosphate) Lyme's
What are the non-pharmacological treatments of RA?
OT/PT - mobility Ax and preservations, work assessment, walking aids
podiatrists - foot clinics, foot wear assessments etc
What are the pharmacological treatments of RA?
symptomatic
NSAIDS, analgesics etc
DMARDS - glucocorticoids, methotrexate, sulfasalazine
biologics - anti TNF (etanercept, infliximab) , anti CD20, anti IL16 etc
Describe juvenile idiopathic arthritis
chronic inflammatory arthropathy
commonest rheumatic disease in childhood
clinical diagnosis with no diagnostic tests
group of diseases
overlap with adult inflammatory arthropathies
important differences in children
What name is given to RA in children?
rheumatoid factor positive polyarthritis
What name is given to ankylosing spondylitis I’m children?
enthesitis related arthritis
What is an enthesis?
insertion of - tendon ligament joint capsule fascia - to bone
What is associated with reactive arthritis?
conjungtivitis
urethritis
plantar fasciitis
arthritis
Describe seronegative arthritis
asymmetrical
large lower limb weight bearing joint
(AS/ERA/Reactive / OBD
large and small joint (psoriatic)
Describe seropositive arthritis
symmetrical
large and small joints
wrists and MCPS
often widespread
What tests should be carried out in JIA?
FBC and differential
acute phase response
MRI
think why before - X-rays, synovial biopsies, ANA, rheumatoid factor
What does tiny TIM for?
Trauma
inflammation - infecition, autoimmmune JIA
Malignancy -leukaemia, bone tumours
