Wk11 - MSK Flashcards
(197 cards)
1
Q
Function and structure of a tendon
A
Tendon – Transmits force from muscle to achieve movement
Parallel collagen fibrils with tenocytes
Surrounded by paratenon / sheath
Largely avascular, nutrition via paratenon
As avascular - slow to heal
2
Q
How does tendinopathy occur
A
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
3
Q
Risk factors for tendinopathy
A
Age - more middle age (elderly tend to less activity)
Chronic Disease
Diabetes, Rheumatoid Arthritis
Adverse Biomechanics
Repetitive Exercise
Recent increase in activity
Quinolone 9e.g. ciprofloxacin Antibiotics
4
Q
Pathology of tendinopathy - what happens
A
Probably not inflamation – tendinosis not tendinitis
Deranged collagen fibres / Degeneration with a scarcity of inflammatory cells (Astrom and Rausing 1995)
Increased vascularity around the tendon
Failed healing response to micro tears
Inflammatory mediators released IL-1, NO, PG’s – cause apoptosis, pain and provoke degeneration through release of matrix metalloproteinases
5
Q
Common sites of tendinopathies
A
Achilles Tendinopathy Rotator cuff tendonitis Tennis Elbow (Lateral epicondylitis) Golfers Elbow (Medial epicondylitis) Patella Tendinopathy Hamstring tendonitis Adductor tendonitis Plantar fasciitis
6
Q
Clinical features of tendinopathy
A
Pain
Swelling
Thickening
Tenderness
Provocative tests - Contract that msucle group against resistance
7
Q
Diagnosis of tendinopathy
A
X-ray? - Excludes bone pathology
Ultrasound
MRI – Tendinopathy best seen on T1.
8
Q
Non-operative Tx of tendinopathy
A
NSAID’s
Activity modification
Physiotherapy – stretching , eccentric exercises
GTN patches
PRP injection - To bring extra growth factors into area –> promote healing
Prolotherapy – irritant injection, dextrose (The dextrose will stimulate inflammation to try get tendon to begin healing)
Extracorporeal Shockwave Therapy
Topaz – radiofrequency coblation
Steroid injection – controversial, avoid intrasubstance, ?avoid suppressing inflammatory and healing response (Steroid injection is avoided most of the time - risk of tearing the tendon)
Etc etc
9
Q
FEatures of physiotherapy for tx of tendinopathy
A
Eccentric loading
Contraction of the musculotendinous unit whilst it elongates
Beneficial in approx 80%
10
Q
GTN patches for Tx of tendinopathy
A
¼ patch 125 mcg
Vasodilator - Increases local perfusion
Takes up to 12 weeks to see effects (compliance is often a problem)
Side effects - headaches
11
Q
Extra corporeal shockwave therapy for tx of tendiopathy
A
3 weekly treatments
Approx 75% improve
Breaks down calcification and stimulates healing of underlying problem
12
Q
Operative treatment of tendinopathy
A
Debridement
Excision of diseased tissue
Possible to debride 50% of tendon without loss of function
(Tendon transfers)
13
Q
Definition of compartment syndrome
- Common sites
A
Elevated interstitial pressure within a closed fascial compartment resulting in microvascular compromise
Common sites - leg, forearm, thigh
Orthopaedic emergency - loss of function, limb or life
14
Q
Causes of compartment syndrome
A
Internal Pressure Trauma – fractures, entrapment Bleeding Muscle oedema / myositis Intracompartmental administation of fluids / drugs Re-perfusion – vascular surgery
External compression Impaired consciousness / protective reflexes Drug / alcohol misuse Iatrogenic Positioning in theatre - lithotomy Bandaging / casts Full thickness burns
Combination
15
Q
Pathophysiology of compartment syndrome
A
Pressure within the compartment exceeds pressure within the capillaries
Muscles become ischemic and develop oedema through increased endothelial permeability
Necrosis begins in the ischaemic muscles after 4 hours
Ischaemic nerves become neuropraxic. This may recover if relieved early, permanent damage may result after as little as 4 hours
Compromise of the arterial supply – late
Increased pressure Increased venous pressure 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.
16
Q
Effects of ischaemia of limbs at different time zones
A
1 hour
Nerve conduction normal, Muscle viable
4 hours
Neuropraxia in nerves - reversible
Reversible Muscle ischaemia
8 hours
Nerve axonotmesis and irreversible change
Irreversible muscle ischaemia and necrosis
17
Q
End stage compartment syndrome
A
Stiff fibrotic muscle compartments
Impaired nerve function
Clawing of limbs
Loss of function
18
Q
Diagnosis of compartment syndrome
A
Clinical Diagnosis
History
Examination
Pulses present (until late stages) unless associated vascular injury
Parasthesia and paralysis – usually later. Deep nerves affected first
1st Dorsal webspace
Impaired conscious level
Compartment pressure measurement
Normal pressure 0-4 mmHg, 10mmHg with exercise
DBP-CP <30mmHG = diagnostic
CP>30mmHG = diagnostic
19
Q
Clinical features of compartment syndrome
A
Pain – out of proportion to that expected from the injury
Pain on passive stretching of the compartment (E.g. moving the tones or bending the fingers)
Pallor
Parathesia
Paralysis
Pulselessness (late sign)
20
Q
Urgent treatemtn of compartment syndrome
A
Open any constricting dressings / bandages
Reassess
Surgical release
Later wound closure
Skin grafting / Plastic surgery input
21
Q
If urgent treatment nor enough…
A
Surgical Release:
Full length decompression of all compartments
Excise any dead muscle
Leave wounds open
Repeat debridement until pressure down and all dead muscle excised
Wound closing/skin grafting
22
Q
Compartments of the forearm
A
Flexor
Extensor
Mobile Wad of three
23
Q
Compartment of the leg
A
Anterior
Lateral
Deep posterior
Superiffical posterior
24
Q
Compartments of thigh
A
Anterior
Abbductor
Posterior
25
Peri-operative management of compartment syndrome
```
Adequate hydration
Fluid loss
Monitor and regulate electrolytes (K+)
Correct acidosis
Myoglobinuria
Renal function
```
26
Late presentation/ diagnosis of compartment syndrome
Irreversible damage already present
Fasciotomy will predispose to infection
Consider non-operative treatment
Splint in position of function
27
FEatures of septic arthritis
pain, fever, swollen joint, loss of function
28
Causative organisms of septic arthritis
Staphylococcus aureus (Staph auereus - most common (60-75%) - MRSA emerging problem), Neisseria gonorrhoea, Haemophilus influenzae (children)
Increased risk if steroids, rheumatoid arthritis
Suspected septic arthritis is a medical emergency
29
What are the 3 main classficiation of bone tumours
secondary tumours in bone : very common
myeloma : common, commonest primary bone tumour
primary bone tumours : rare
30
What type of cancers commonly metasasise to bone
metastatic carcinoma
bronchus, breast, prostate, kidney, thyroid (follicular)
childhood
neuroblastoma, rhabdomyosarcoma
Typically goes to bones with a good blood supply - long bones (femur and humorus), vertebrae
31
Presentation of metastases to bone
```
often asymptomatic
bone pain
bone destruction
long bones : pathological fracture
spinal metastases: vertebral collapse, spinal cord compression, nerve root compression, back pain.
hypercalcaemia
```
32
What type of imaging is useful for picking up metasasis on bone
PET CT
33
2 types of bone metastasis
Lytic V sclerotic bone mets
| Majority are lytic
34
Sites from which sclerotic metastasis to the bone occurs
```
prostatic carcinoma
breast carcinoma
carcinoid tumour (neuroendocrien tumour)
sclerotic on x-ray
reactive new bone formation, induced by tumour cells
```
35
2 tumours that produce solitary bone metastases
Renal and thyroid carcinomas
- often longer survival
- surgical removal often valuable
36
Features of myeloma
Commonest malignant primary bone tumour
Neoplasmic monoclonal proliferation of plasma cells
solitary (plasmacytoma) or multiple myeloma
orthopaedic consequences
“medical” consequences (as can get in bone marrow)
37
Clinical effects of myeloma
- Osteolytic bone lesions (lytic 'punched out' lesions) - backaches, pathological fractures and vertebral collapse
- Hypercalcaemia
- Anaemia, neutropenia or thrombocytopenia
- Recurrent bacterial infections
- Renal impairment
Immunoglobulin excess
- ESR > 100 (can be diagnostic)
- serum electrophoresis : monoclonal band (diagnostic)
- urine : immunoglobulin light chains (Bence Jones protein) (diagnostic)
2 types of light chains in plasma - Kappa and Lambda
If have myeloma - only have one type - either Kappa or Lambda - as monoclonal proliferation
38
Light chains present in plasma and yeloma
2 types of light chains in plasma - Kappa and Lambda
| If have myeloma - only have one type - either Kappa nad Lambda - as monoclonal proliferation
39
Marrow replacement (due to myeloma) results in
Renal impairment with myeloma
pancytopenia
anaemia
leucopenia: infections
thrombocytopenia: haemorrhage
Myeloma kidney: precipitated light chains in renal tubules
Hypercalcaemia
Amyloidosis
40
The types of primary bone tumours
Benign
- Osteoid osteoma
- Chondroma
- Giant cell tumour
Malignant
- Oesteosarcoma
- Chondrosarcoma
- Ewing's tumour
41
Features of osteoid osteoma
A small, benign osteoblastic proliferation
Common, any age especially adolescents, M:F 2:1
Any bone, especially long bones, spine
Pain, worse at night, relieved by aspirin, scoliosis
juxta-articular tumours : sympathetic synovitis
Tx - radio-frequency ablation
42
Features of osteosarcoma
- definition
- epidemiology
A malignant tumour whose cells form osteoid or bone
Age : peak 10 -25
Site : metaphysis of long bones, 50% around knee
Sex : male preponderance, 3:2
Incidence : 2-3 / million / year (not very common)
Classic presentation - pain, swelling (shoulder), inability to move a limb
highly malignant
early lung metastases
5 year survival : 15-20% pre-chemotherapy
modern survival : 50-60%
Tumour can often produce a new cortex of bone --> forming a codman's triangle
Image guided biopsy - by ultrasound or CT
8 weeks of chemotherapy, surgery to remove tumour, often have another 8 weeks of chemotherapy if responded well
43
Worse prognosis of osteosarcoma - a variant
Paget’s
multifocal
post-irradiation
Pagets disease:
Common in elderly, Anglo-saxon origin
Disorder of excessive bone turnover
Increased osteoclasis, increased bone formation, structurally weak bone
Disorganized bone architecture (often in vertebrae, pelvis, skull, femur)
Usually lytic
- bone pain
OA, deafness, spinal cord compression, high cardiac output - cardiac failure, pagets sarcoma (aggressive form of osteocarcinoma)
44
Name the common cartilaginous tumours
Benign: Enchondroma, Osteocartilaginous exostosis
Malignant: Chrondrosarcoma
45
Features of enchondroma
Lobulated mass of cartilage within medulla
Common, any age.
>50% hands and feet, long bones.
Often asymptomatic in long bones.
Hands - swelling, pathological fracture.
Low cellularity, often surrounded by plates of lamellar bone
46
Features of osteocartilaginous exostosis
Benign outgrowth of cartilage with endo-chondral ossification,
Probably derived from growth plate
Very common, usually in adolescence
Uncommonly multiple-diaphyseal aclasis, autosomal dominant
Metaphysis of long bones, not cranio-facial
47
Features of chondrosarcoma
de novo (primary) or from a pre-existing enchondroma or exostosis (secondary)
Central,within the medullary canal or peripheral on bone surface
10% of malignant primary bone tumours
predominantly middle aged and elderly
Males: females; 2:1
axial skeleton, pelvis, ribs, shoulder girdle proximal femur and humerus. Hands and feet rare
48
Main difference between chondrosarcoma and osteosarcome
-
49
Features of Ewins
Malignant primary bone tumour seen in children - peak 5-15 years
long bones (diaphysis or metaphysis)
flat bones of limb girdles
early metastases to lung, bone marrow and bone
Historical 5 year survival of 5%
Modern 5 year survival 50-60%
Often tibia, fibia or pelvis
Responds well to radio and chemotherapy
50
Diagnosisng ewins
Stain it for C99 (/) - also do molecular geentics - has a specfic translocation (11 to 22)
51
Differentials of an acute hot joint
Septic arthritis
Crystal arthropathy
Trauma/haemarthrosis
Early presentation of polyarthropathy (RA, PsA)
52
Routes by which bacteria can reach the joint (--> septic arthritis)
1. The hematogenous route
2. Dissemination from osteomyelitis
3. Spread from an adjacent soft tissue infection
4. Diagnostic or therapeutic measures.
5. Penetrating damage by puncture or trauma
53
Investigations for septic arthritis
Joint aspirate - microbiology for gram stain and culture
Blood culture
FBC - leucocytosis
X-ray - of no value
54
With septic arthritis the synovium is inflamed with...
fibrin exudation and numerous neutrophil polymorphs
55
Other specific types of septic arthritis
Lyme disease - borrelia burgdoferi
Brucellosis
Syphilitic arthritis - congenital and acquired
56
Features of crystal arthropathy
Gout and Pseudogout
Excess levels of uric acid
Leads to deposition of urate crystal in joints or soft tissue (tophi)
Acute gout - precipitation in joint stimulated acute inflammatory process
Chronic gout - tophi formation
57
How is gout diagnosed?
| Feature of primary and secondary gout
Hisotry - rapid onset pain, swelling, tenderness, max intensity within 6-12 hours
Diagnsoed by aspirate - negatively birefringent needel shaped cyrstals in polarized microscopy
Serum urate levels and U&Es
Definitive diagnosis = MSU crystals
Primary - hyperuricaemia due to genetic predisposition e.g. Lesch-Nyhan syndrome
Secondary - high uric acid due to myeloproliferative disorder (PCRV), leukaemia treated by chemo, thiazides, chronic renal disease
58
Where is the most common site affected by gout?
```
1st metatarsal (big toe)
Podagra - inflammation of 1st metatarsal joint - classical presentation of gout
```
59
Management of gout (both acute and chronic)
Acute:
NSAIDs - high doses rapipdly reduce pain and swelling
Cochicine - works best when initiated within 24 hours of attack; works in several ways e.g. IL-1 interference, microtubule interference; Need to stop statins with cochicine treatmen
Corticosteroids
Long term:
Aim SUA <300 using ULT (urate lowering therapy)
Emphasise lifestyle alterations
Allopurinol - excrteed renally; ; Xanthine oxidase inhibitor; Risks include DRESS syndrome - occurs wihtin first few months usually, particulalry HLA mutations at risk
FEbuxostat - XO inhibitor, hepatic metabolism, very expensive (20x allopurinol)
Uricosuric agent (probenecid) - increases secretion of uric acid into urine
Rasburicase - given via IV - progressive risk of anaphylaxis, recombinate urate oxidase
60
Management of pseudogout
Aspiration helps reduce the pain and swelling
NSAIDs
Colchicine
61
Features of reactive arthritis
Sterile synovitis which occurs following an infection
Trigger organisms - salmonella, shigella, yersinia, chlamydia thrachomatis
Preceding illness usually a urethritis or diarrhoral
Association with HLA B27 (75%)
62
Clinical features of reactive arthritis
Acute, asymmetrical lower limb arthritis
More common in men
Days - weeks post infection
Asymetry oligoarthritis, larger jiont of lower limbs, daylitis, enthesitis (e.g. plantar fasciitis), bursitis, onjuctivits/uveitis, circinate balanitis, mouth ulcers, conjuctivities, keratoderma blenorrhagica (dark rash on base of foot)
63
Management of reactive arthritis
Little evidence that treating the triggering infection alters the course of the disease
Pain control - NSAIDs, intra-articular steroids
64
Prognosis of reactive arthritis
Usually self limited, lasts up to 6 months
May be chronic
Very occassionally there may be cardiac complications e.g. aortic regurgitation, aortitis, and amyloidosis
65
Features of enteropathic arthritis
Form of reactive synovitis seen in association with UC and Crohn's disease
An asymmetrical lower limb arthritis
Treatment of the bowel disease and NSAIDs
66
# Define OA
Features of osteoarthritis
Definition: Degenerative joint disease involving loss of articular cartilage, influenced by mechanical and biological factors.
```
Degenerative joint disease
Commonest form of arthritis
Middle aged/elderly
Weightbearing joints - hip, knee
Pathology - disorder of articular cartilage
```
Primary generalized - multiple joints, hands
Secondary - fracture, previous sepsis, RA, osteonecrosis, CDH, steroids, chronic overuse, gout, haemochromotosis, ochronosis, peripheral neuropathy
67
Signs and symptoms of osteoarthritis
Differential diagnosis of OA
Ix/Tx of OA
Pain and stiffness - worse at end of day
Cerpitations
Reduced ROM
Loss of articular cartilage, exposure of underlying bone, subchondral cysts and slcerosis, osteophytes
Synovium becomes hyperplastic, mild inflammation, bony detritus
Differential diagnosis:
bursitis, gout/pseudogout, RA, PA, AVN, meniscal tear
```
X-ray - LOSS
Bloods
Exercise
Physio/OT
NSAIDs + paracetamol
Steroid injection
Arthroplasty
```
68
Function of bone
Structural - support, protection, movement
| Mineral storage - calcium and phsophate
69
Structure of bone
```
Cortical bone:
Compact or tubular bone
80% of the skeleton
Slow turnover rate/ metabolic activity
Higher Young's modulus and resistance to torsion and bending
```
Cancellous bone:
Spongy or trabecular bone
Higher turnover rate and undergoes greater remodelling
Lower YOung's modulus, and is correspondingly more elastic
Composition - Matrix & Cells
Matrix:
Organic - collagen, non-cllagenous proteins, mucopolysaccharides
Inorganic - calcium, phosphorus
Cells: Osteoprogenitor, osteocyte,, osteoblast, osteoclast
Diaphysis (shaft)
Epiphysis (end)
Metaphysis (transitional flared area between diaphysis and epiphysis)
70
Features of physis of bone
Unique feature of children's bone
Responsible for skeletal growth
Allows remodelling of angular deformity after fracture
If physeal blood supply damaged, will lead to growth arrest (either partial or complete)
71
Stages of indirect fracture healing
1. Fracture haematoma and inflammation:
Blood from broken vessels forms a clot.
6-8 hours after injury
Swelling and inflammation to dead bone cells at fracture site.
2. Fibrocartialge (SOFT) callus:
(lasts about 3 weeks)
New capillaries organise fracture haematoma into granulation tissue - 'procallua'
Fibroblasts and osteogenic cells invade procallus.
Make collagen fibres which connect ends together
Chondrocytes begin to produce fibrocartilage
3. Bony (HARD) callus
(after 3 weeks and lasts about 3-4 months)
Osteoblasts make woven bone
4. Bone remodelling
Osteoclasts remodel woven bone into compact bone and trabecular bone
- Often no trace of fracture line on X-rays
72
Stages of direct fracture healing
Unique 'artifical' surgical situation
Direct formation of bone (via osteoclastic absorption and osteoblastic formation), without the process of callus formation, to restore skeletal continuity.
Relies upon compression of the bone ends
No callus
Cutting cones cross fracture site
Lay down new osteones
73
Blood supply to bones
Endosteal - inner 2/3rds
Periosteal - outer 1/3rd
Injured by a fracture
Further damaged by surgery
74
Certain fractures are prone to problems with union or necrosis because of potential problems with blood supply... e.g.
Proximal pole of scaphoid fractures
Talar neck fractures
Intracapsular hip fractures
Surgical neck of humerus fractures
75
What patient factors can inhibit fracture healing?
```
Increasing age
Diabets
Anaemia
Malnutrition
PVD
Hypothyroidism
Smoking
Alcohol
```
76
What medications can inhibit fracture healing
NSAIDs (COX 2 NSAIDs inhibit fracture healing more than non-specific NSAIDs)
Steroids
Bisphosphonates (Inhibit osteoclastic activity; Delay fracture healing as a result; Long half-life
77
Epidemiology of RA
FEmales:males 3:1
Clusters in families
If 1st degree relative affected, 2-10 times greater risk
78
Aetiology of RA
HLA-DR4 and other genetic factors
Smoking - definite, multiple studies, ACPA
Infection (EBV< TB, prophyromonas gingivalis)
Hormonal (pregnancy, female prepond)
(Rheumatoid can go into remission with pregnancy and then flares again after pregnancy)
79
Risk factors for RA
Genetic risk factors (60% of risk0
- Susceptibility genes (e.g. HLA-DRB1)
- Epigenetic modifications
Non-genetic risk factors (40% of risk)
- Smoking
- Microbiota
- Female sex
- Western diet
- Ethnic factors
80
Pathophysiology of RA
```
Synovitis = immune cells invading a normally relatively cellular synovium in the form of a pannus
Pannus = hyperplastic, invasive tissue leading to cartilage breakdown, erosions and consequent reduced function
```
81
What is the first area where erosions occur in rheumatoid?
The synovial lining = the bare area
| And moves in from the margins
82
Clinical features of RA
Synovitis - any synovial joint
Symmetrical
Small jts hands and feet early on; shoulder/hip at onset rare
MCPs/PIPs/wrists
Inflammatory - pain, erythema, swelling, EMS
Tenosynovitis, bursitis, CTS
Constitutional sx: fatigue, weakness, low grade fever, weight loss, anorexia
83
Joint features - late signs of RA
```
Boutonniere
Swan neck
Z-thumn (Boutonniere of thumb)
Volar subluxation of wrist
Ulnar deviation of digits
Radial deviation wrist
Paino key ulnar head
```
84
Extra-articular features of RA
Respiratory - e.g. pulmonary fibrosis
Cardiac - e.g. pericarditis
Dermatological - Rheumatoid nodules, thinning, ulceration
Ophthalmic - scleritis, keratoconjunctivitis
Neurological - carpal tunnel syndrome, peripheral neuropathy
Haematological - anaemia, thrombocytosis
85
RA investigations
Bloods: FBC, U&Es, LFTs, ESR/CRP, RF, ACPA
Rheumatoid factor
Imaging - Xray, MRI
86
Rheumatoid factor
Autoantibody against Fc portion of IgG
Usually IgM against IgG, though can be any isotype
60% sens, 80% spec
other conditions that also show +ve RF = SLE, SBE, TB, EBV etc.
Part of assesment but is not diagnostic
87
Anti-CCP/ACPA
Newer antibody than RF
Sens 60%, spec 80-90%
Picks up those who may be RF -ve.
Predictor of worse prognosis, more erosions, resistant disease
Linked with smoking (increases citrullination)
88
Imaging for RA
X-rays: Soft tissue swellign, joint spcae narrowing, erosions, periarticular OP
USS: more sensitive for synovitis and erosions
MRI: bone marrow oedema
89
Differentials of RA
OA, SLE, PMR, psoriatic arthropathy, reactive arthritis, sarcoid, Lyme's
90
Treatment of RA
Non-pharmacological:
OT/PTc(mobility help, walking aids etc.), Podiatrists (specialty foot assessment, footwear adjustments). Dieticians
```
Pharmacological:
Symptomatic
- NSAIDs, Analgesia etc.
DMARDs:
- Glucocorticoids (oral, IA, IM)
- Biologics (anti-TNF, anti-CD20, anti-IL6 etc)
```
91
How does Methotrexate (a DMARD) work in the Tx of RA
| - Side effects
```
MTX is a systemic immunosuppressant (1 mark). MTX stops the actionof the enzyme dihydrofolate (1 mark) needed for production of DNA
Is a Dihydrofolate reductase inhibitor
7.5mg-25mg per week orally
Common side effects - GI, hair, skin, rashes
Serious side effects: lungs, liver, BM
Concomitant folic acid
Pregnancy - total contraindication
Withhold during infection and if on abx
(Can't give with trimethoprim)
```
92
How does Sulfasalazine (a DMARD) work in Tx of RA?
```
MOA
Salazyopyrin and mesalazine (5-ASA)
RA, IBD etc.
500mg-4g OD orally
Common side effects: GI, rashes
Serious side effects: BM
Safe in pregnancy
Fine in infection unless cytopenic (cf guidelines)
```
93
Name the biologics used to treat RA
Anti-TNF:
Etanercept, infliximab, adalimumab, golimumab, certolizumab
TB, infection risk, MS, CHF
Anti-CD20 (depletes T cell, reduces immunoglobulin levels)
Rituximab
Infection, PML, Hypogammaglobulinaemia
Anti-IL6:
Tocilizumab
Minimal CRP, infections, high lipids
CTLA4-Ig:
Abatcept
Infections
JAK inhibitors:
Tofacitinib and others e.g. Baricitinib
High lipids, infections esp VZV, reduced CRP
94
SLE epidemiology
Commoner in Afro-Caribbean, South Asian, Mexican populations
Female preponderance
Symptom onset commonly during reproductive years
Diagnosed 40-50 years
Premature death - average 25 years earlier - infection, cardiovascular disease, ESRF
95
Diagnosing SLE
ACR classification criteria
- Malar rash
- Discoid rash
- Photosensitivity
- Oral ulcers
- Non-erosive arthritis
- Pleurisy or pericarditis
- Renal
- Neurological
- Haematological
- Immunological
- Positive ANA
At least 4 criteria needed for the classification of SLE (don't need to have them at the same time)
SLICC classification:
Need at least 1 clinical and 1 serological manifestation (need 4 in total)
Diagnosis possible with just biopsy proven LN and positive immunology
Less specific
96
Problems with ACR criteria (used for diagnosing SLE)
Classification rather than diagnositc criteria
Subset of the clinical manifestations - seizure and psychosis only induced for NPSLE; Proteinuria and casts only renal criteria (renal biopsy not included)
97
Clinical presentation of SLE
```
Variable
Mild to severe disease
Common features:
- Constitutional symptoms (fatigue)
- Cutaneous manifestations
- Arthralgia and arthritis
```
98
Musculoskeletal manifestations with SLE
Inflammatory arthritis
Jaccoud's arthropathy (ligaments are loose but no erosive properties)
AVN - seen out with steroid use
Fibromyalgia
Osteoporosis
99
Renal involvement with SLE
20% will develop ESRF in 10 years
Typically presents within first year or two
Urinalysis, U&E, BP monitored at clinic
ds-DNA - if have level more likely to have renal involvement
Renal biopsy helpful for diagnosis, prognosis and determining treatment
100
Pulmonary effects from SLE
```
Pleurisy
Pleural effusions
Acute pneumonitis
Diffuse alveolar haemorrhage
Pulmonary hypertension
Shrinking lung syndrome
```
101
Cardiovascular effects from SLE
```
Pericarditis +/- effusion
Myocarditis
Vavular abnormalities
Cornoary heart disease - high risk of morbidity and mortality long-term
Risk of MI 50x
```
102
Neuropsychiatric effects from SLE
```
Headache (constant)
Anxiety and mood disorder
Seizure
Demyelination
GBS
Mononeuritis
```
```
Requires tailored investigation
EEG
MRI
LP
Psychiatric evaluation
```
Anti-ribosomal P
Associated with mood disorders
103
Gastrointestinal involvement with SLE
```
Rare
Dysphagia
Reduced peristalsis
Peritonitis
Pancreatitis
Lupus hepatitis
```
104
Haematological involvement with SLE
Anaemia of chronic disease
Autoimmune haemolytic anaemia
Thrombotic thrombocytopenic purpura (TTP) – MAHA, low plts, fever, neuro/renal involvement - check aPLS antibodies
Leukopenia
Can have associated lymphadenopathy and splenomegaly
Thrombocytopenia
- Mild or ITP
105
ANA
Present in 95-98% of patients
SLE results due to activation of innate and adaptive immunity
Interaction of self antigens on or released by apoptotic cells
Sensitive but not specific
5% healthy population have positive ANA – need clinical context
106
ENA
If ANA positive, helpful to know which antigens affected
```
Ro/La – SLE, Sjogrens
Ds-DNA – SLE
Sm - SLE
RNP – mixed CTD
Centromere – limited SScl
Scl-70 – diffuse SScl
Histone - drug induced lupus
```
107
Compliment involvement with SLE
```
Complement consumption in active disease
C3 more specific
C4 can be chronically low
Trends more important than absolute numbers
> 90% negative predictive value
```
108
Investigation for suspected SLE
3 medications for SLE
- FBC - leukopenia
- U&Es - looking for renal manifestations
- Urinalysis - for renal manifestations
- ESR/CRP
- Activated PTT
- ANA
○ Best diagnostic test and is positive in virtually all patients with SLE
○ Clinically relevant ANAs are IgG antibodies
○ Can also be positive in other connective tissue disease e.g. RA, systemic sclerosis, Sjogren's syndrome, thyroid disease
- CXR - if has cardiopulmonary symptoms - looking for pleural effusion etc.
- ECG - if has cardiopulmonary symptoms
In the UK 3 medications are licensed:
- Steroids
- Hydroxychloroquine
- Belimumab
109
Treatment of mild disease of SLE
Cutaneous disease – topical therapies, UVA/UVB sunblock
MSK – NSAIDS, IA/IM steroid, low dose oral prednisolone, HCQ +/- MTX
Serositis – NSAIDS, MTX
110
Treatment of moderate disease of SLE
Treatment as per mild disease plus:
Oral prednisolone (0.5mg/kg)
MTX, Aza, MMF, Ciclosporin, Tacrolimus
Belimumab
Refractory disease – Rituximab
111
Treatment of severe disease of SLE
Treatment as per mild and moderate disease activity plus:
High dose steroid
DMARDs
B cell therapy
Cyclophosphamide
IVIG – Refractory cytopenias, TTP, Catastrophic APLS
Plasmapheresis – TTP, Catastrophic APLS, Diffuse alveolar haemorrhage, Refractory NPSLE or LN
112
Adjunctive therapy for SLE
Topical lubricants for sicca symptoms
Fatigue management groups
Calcium channel blockers for Raynauds
Treatment of co-existent Fibromyalgia
CVS risk
Osteoporosis risk
Co-existent APLS: Anticoagulation in confirmed thromboembolic disease. Use of antiplatelets debatable
113
What is vasculitis?
Inflammation of blood vessels
Skin, kidneys, lungs, joints, nerves, ENT
It is an autoimmune reaction
114
What are the different types of vasculitis?
Large vessel vasculitis
Medium vessel vasculitis
ANCA-Associated Small Vessel Vasculitis
Immune complex Small Vessel Vadculitis
115
Subtypes of Large Vessel Vasculitis
Takayasu Arteritis
| Giant Cell Arteritis
116
Features of giant cell arteritis
Systemic vasculitis that affects the aorta and its major branches
Prevalence increases with advancing age - Peak incidence between 70-79 years
Female:Male ratio 2-3:1
117
Clinical presentation of giant cell arteritis
```
Headache - temporal headache with tenderness, subacute onset, constant, little relief with analgesics
Visual symptoms
Jaw claudication
Polymyalgia rheumatica symptoms
Constitutional upset
```
118
Complications of GCA
1) Visual loss
- Acute ischaemic optic neuropathy
- Sudden painless loss of vision, occassionally preceded by amaurosis fugax
2) Large vessel vasculitis
- Vascular stenoses nad aneurysms
3) CVA
- Obstruction or occlusion of internal carotid artery or vertebral arteries
119
Diagnosing GCA
Clinical presentation - typical headache, appropriate age, associated clinical features - jaw claudication , constitutional symptoms, PMR
Clinical examination findings - temporal artery asymmetry, thickening, loss of pulsatility
Acute phase response - ESR/CRP
Further investigations
120
Investigations for GCA
Temporal artery biopsy - Gold standard: Interruption of internal elastic laminae with mononuclear inflammatory cell infiltrate within vessel wall. Multinucleated giant cells are typical (40-60%) but their absence does not exclude a diagnosis.
Temporal Artery USS
MRI
PET CT
121
Treatment of GCA
1mg/kg/day prednisolone (max 60mg) for 1 month
Taper to 15mg by 12 weeks
IV methylprednisolone if visual symptoms
Aim to discontinue corticosteroids by 12-18 months
Aspirin 75mg daily - reduces ischaemic complications
122
Differential diagnosis for cutaneous (small vessel) vasculitits
Idiopathic
Drugs
Infection: HCV, HBV, gonococcus, meningococcus, staph.
Secondary RA/CTD/PBC/UC
Malignancy
Manifestation of small/medium vessel ANCA associated vasculitis
123
FEatures of Henoch-Schonlein Purpura (HSP)
```
Small vessel vasculitis
More common in children, 2-11y
Observed in adults, mean age 43y
Male > Females
FRequently self limiting illness, 4-16 weeks
Good overall prognosis
Mortality 1-2%
```
124
Clinical features of Henoch Schonlein Purpura (HSP)
Classic purpuric rash: buttocks, thighs>lower legs
Urticarial rash, confluent petechiae, ecchymoses, ulcers
Arthralgia/arthritis (lower limb) in 75%
125
Complications of HSP
Gastrointestinal: pain, bleeding, diarrhoea, rarely intussuseption. More common in children
Renal: IgA nepphropathy, more common in adults
urological: orchitis
CNS: very rare
126
HSP management and prognosis
Often no treatment required
Corticosteroids for certain complciations; testicular torsion, GI disease, occasionally arthritis
Steroids in renal disease: evidence limited. Steroids do not prevent development or progression of renal disease.
127
Clinical presentation of ANCA associated small vessel vasculitis
2 month history of: weight loss, fatigue, joint pain, headaches/facial pain
128
Investigations for ANCA associated vasculitis
FBC
CRP
U&Es
Urine dipstick: +++ protein, + blood
Urine portin: Creatinine ratio (PCR): 30
129
Initial treatment for ANCA associated vasculitis
Intravenous antibiotics
| Intravenous fluids for presumed respiratory tract infection with dehydration
130
Immunology of ANCA associated vasculitis
cANCA stongly positive
| PR3 130 IU
131
Diagnosing ANCA associated vasculitis
GRanulomatosis with polyangitis (GPA):
Characterised by granulomatous necrotising inflammatory lesions of the upper and lower respiratory tract and often a pauci-immune glomerulonephritis
132
GPA: the classic triad of disease
Upper airway/ENT: - rhinitis, chronic sinusitis, chronic ottits media, nasal septal perforation, saddle nose deformity
Lower respiratory: Parenchymal nodules + cavitation, Alveolar haemorrhage
Renal: (rapidly progressive) pauci-immune glomerulonephritis
Constitutional symptoms: Fatigue, weight loss, fever/sweats, myalgia/arthralgia, failure to thrive in elderly
133
Immunological diagnosis of ANCA
Autoantibodies directed against cytoplasmic constituents of neutrophils and monocytes
2 means of testing:
- Indirect immunofluorescence
- ELISA for PR3/MPO
Looking for cANCA and pANCA
134
cANCA with PR3 suggesstive of...
GPA
135
pANCA with strong MPO suggestive of...
MPA (or EGPA)
136
2 broad reasons for using immunosuppressant drugs
Abnormal inflammation:
- Inflammatory arthropathies
- Ulcerative colitis/Crohns
- Psoriasis
Unwanted normal inflammation
- Solid organ transplants
- Bone marrow grafts
137
Steroids (e.g. prednisolone) being used for immunnospuressants
& adverse effects
Steroids are excellent immunosuppressants:
Rapid onset (within hours)
Easy to administer
Able to treat wide variety of inflammatory conditions
Limited by intolerable adverse effects, especially at high dose
```
Weight gain and fluid retention
Glaucoma
Osteoporosis
Infection
Hypertension and hypokalaemia
Peptic ulceration and GI bleed
Psychological/psychiatric symptoms
```
138
MOA of corticosteroids
Modulators of transcription factors
Cortciosteroids enter the cell and bind to a glycocorticoid receptor (either in cytoplasm or nucleus) --> will upregulate transcription factors which will promote anti-inflammatory products
139
Examples of non-steroid immunosuppressive drugs
Inhibitors of DNA synthesis:
Methotrexate
Azathioprine
Mycophenolate
```
Lymphocyte signalling inhibitors:
Cyclosporin
Tacrolimus
Sirolimus
Leflunomide
```
140
What are the 2 roles that methotrexate has?
When given as a high does - is a cytotoxic chemotherapeutic agent
Low dose - immunosuppressant
141
MOA of methotrexate
Methotrexate inhibits the folate cycle (has very similar structure to folic acid) and pentose-phosphate pathway --> prevents the development of nucleotides that go into DNA synthesis; therefore preventing DNA synthesis
From 50 drugs database:
Stops the action of the enzyme dihydrofolate needed for production of DNA
142
Methotrexate: effect on cells
Causes cell cycle arrest due to inhibition of DNA synthesis
143
Different cellular functions of methotrexate
```
Folate Antagonism
Inhibiton of adenosine signalling
Inhibits Methyl donors
Eicosanoids and MMPs
Cytokines
Adhesion molecules
```
144
Adverse effects of methotrexate
GI: nausea, vomitting, diarrhoea, hepatitis, stomatitis, hepatotoxicity
Haematological: leukopenia (predisposition to infection, nausea and vomiting)
Kidney failure
Abdominal pain
Birth defects
Others: frequent infections, pulmonary fibrosis
145
What medication is often given alongside methotrexate
Folic acid 5mg usually given 4 days after MTX
| "Methotrexate on Mondays; Folic acid on Fridays"
146
Indications for methotrexate in practice
Most commonly used for rheumatological disease: RA, psoriasis and psoriatic arthropathy
Steroid sparing agent in giant cell arteritis
147
Describe common indications for immunosuppressant drugs and biologic therapies
Autoimmune conditions - IBD, Grave's disease, RA etc.
Post-transplant immunosuppression
Renal vasculitis
Paediatric leukaemia (methotrexate)
148
Mechanism of action of Azathioprine
Blocks purine synthesis, mainly in lymphocytes, disrupting DNA synthesis and therefore blocking continued immune response
149
Side effects of Azathioprine
```
Birth defects
Nausea and vomiting
Hepatitis
Cholestasis
Dizziness/fatigue
Diarrhoea
Leukopenia
Thrombocytopenia
Skin rashes
Anaemia - bone marrow suppression
```
150
Azathioprine metabolsim
TPMT enzyme vital in reducing active drug in cells
A small percentage of people lack this enzyme
Without TPMT there is an accumulation of the most active metabolites of azathioprine within cells and development of severe toxicity
Checking TPMT activity prior to treatment with azathioprine prevents this problem.
151
Indications for Azathioprine in practice
Most commonly used for IBD
| Used in other autoimmune disorders: Myaesthenia Gravis & Eczema
152
Clinical use of Azathioprine in practice
Given orally on a daily basis
Effects take several weeks to become evident
Need to monitor bloods on a monthly basis
153
MOA of cyclosporine
This lowers the activity of T cells by binding to cyclosporin, a protein which facilitates protein binding and regulates activity of other proteins. Inhibition of this inhibits phosphatase activity which is required for activation of transcription factors which up-regulate expression of inflammatory cytokines
154
Side effects of cyclosporin
```
Nephrotoxicity
Hypertension
Hepatotoxicity
Anorexia and lethargy
Hisituism
Gum enlargement
Peptic ulcers
Fever
Vomiting and diarrhoea
Confusion
HYpercholesterolaemia
```
When used in post-renal transplantation, is associated with development of gout
155
What is the drug Tacrolimus?
Different class of drug to cyclosporin but similar MOA.
More potent activity.
Very similar use to cyclosporin but may be a little tolerated
156
Indications for Tacrolimus use in practice
Usually given for organ transplantation - liver, kidney, heart/lung
157
Disadvantages of immunosupressants
Immunosuppressants often insufficient to control inflammatory disease with subsequent progression.
Usually have a slow rate of onset limiting usefulness in acute severe disease
Even at low doses they have significant toxicities
Class effects include: Bone marrow suppression, infections.
158
What route are biologic therapies usually delivered by?
Parenteral
159
Know the features of mechanical back pain
This is non-specific low back pain, accounting for 97% of back pain
Onset at any age and generally worsens with movement or prolonged standing - early morning stiffness for less than 30 minutes
160
Causes of mechanical back pain (non-specific lower back pain)
Lumbar strain/sprain is most common cause
Degenerative discs/facet joints - Degenerative disc disease is spondylosis (asymptomatic/pain increases with flexion, sitting and sneezing); Degenerative facet disease (more localised pain, increased with extension)
Disc prolapse/spinal stenosis
Compression fractures - common in elderly patients
161
What are the 3 broad differentials of back pain
1. Mechanical (97%)
2. Systemic - infection, malignancy, inflammatory
3. Referred (i.e. no pathology in the back)
162
Non-specific LBP management
Education, promote self-management --> advise to stay active
Exercise programme and physiotherapy
Analgesics as appropriate (avoid opiates)
Also acupuncture
163
Mechanical back pain - radiculopathy
Disc prolapse: Herniated nucleus pulposus:
May be acute, increase cough
Typicaly leg> back pain; sciatica is the most common nerve affected
Leg pain = dermatomal distribution
Straight leg raising test +ve
Reduced reflexes
Most resolve spontaneously within 12 weeks
Wait 12 weeks before doing MRI scan
164
Mechanical back pain - 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
Only operate on those whose symptoms are getting worse and worse
Neuropathic agents used e.g. gabapentin
165
Features of cauda equina syndrome
Spinal cord ends at L1/2 (need to do lumbar puncture below this)
Neuropathic symptoms - bilateral sciatics, saddle anaesthesia
Bladder or bowel dysfunction - reduced anal tone (need to test perianal sensation and anal tone)
usually a large prolapsed disc
Urgent neurosurgical review
166
Mechanical back pain - spondylolisthesis
```
'Slip' of one vertebra on the one below:
Pain may radiate to posterior thigh
Increased pain with extension
Born with defect (?)
Often found incidentally on imaging
Often asymptomatic
Rarely needs surgery (only if severe)
```
167
Mechanical back pain - compression fracture
Elderly patient
Often sudden onset, severe
Radiates in 'belt' around chest/abdomen
most pain settles in 3/12; chronic mechanical and kyphosis
Associated osteoporosis - risk of recurrence high
Investigations - x-ray, DEXA scan
Treatment:
Conservative (analgesia)
Vertebroplasty (cement) or kyphoplasty (balloon)
168
Referred pain in back
Retroperitoneal structures:
Aortic aneurysm - CVS features (BP, inc. HR), collapse
Acute pancreatitis - epigastric pain, relief lean forwards, unwell
Peptic ulcer disease (duodenal) - epigastric pain (meals), history PUD, vomit, blood/malaena
Acute pyelonephritis/Renal colic - history UTI/stones, unwell, radiation, haematuria, frequency
Endometriosis/gynae
169
Systemic causes of back pain
Infection - discitis, osetomyelitis, epidural abscess
Malignany
Inflammatory
170
Features of infective discitis
High index of suspicion
Fever (may be PUO), weight loss
Constant back pain - rest, night pain
Immunnosppuressed, diabetes, IV drug use
```
Bloods: FBC, ESR, CRP, blood cultures
Imaging xray, MRI
Radiology-guided aspiration
Most common Staph aureus
IV antibiotics +/- surgical ddebridement
Look for source
```
171
Malignancy causing back pain
History of malignancy: "LP Thomas Knows Best" - Lung, prostate, thyroid, kidney, breast
Onset age >50 years
Constant pain, often worse at night
Systemic symptoms, primary tumour signs and symptoms
X-ray (lytic/destructive), MRI, bone scan
Look for primary site
172
Inflammatory back pain (IBP)
Onset <45 years (often teens)
Early morning stiffness >30 mins
Back stif after rest and improves with movement
May wake 2nd half of night, buttock pain
173
Approach to investigating back pain
History (red flags)
Examination - back, neurology, abdomen
Most = non-specific LBP = No further investigation
Keep diagnosis under review - investigate if unusual/new features
Imaging - x-ray, MRI
Bloods - if suspect infective/inflammatory, myeloma screen
174
Red flags for back pain
```
Symptoms:
New onset <16 or >50
Following significant trauma
Previous malignancy
Systemic = fevers/rigors, general malaise, weight loss
Previous steroid use
IV drug abuse, HIV or immunosuppressed
Recent significant infection
Urinary retention
Non-mechanical pain (worse at rest "night pain")
Thoracic spine pain
```
```
Signs:
Saddle anaesthesia
Reduced anal tone
Hip or knee weakness
Generalised neurological deficit
Progressive spinal deformity
```
175
Yellow flags for back pain
```
Bio-psycho-social model = patients likely to develop chronicity:
ABCDEFW
Attitudes
Beliefs
Compensation
Diagnosis
Emotions
Family
Work relationship
```
176
Mechanical vs Inflammatory back pain
Age of onset - Any age (M); Usually <40 yrs (I)
Onset - Variable, may be acute (M); Insidious (I)
Morning stiffness - <30 mins (M); >30 mins (I)
Exercise: May worsen pain (M); Improves pain (stiffness) (I)
Rest - Often improves (M); No improvement (I)
Night - May imporve (M); May wake during second half of night (I)
177
Features of ankylosing Spondylitis
A type of inflammatory back pain.
Low back pain and stiffness for more than 3 months which improves with exercise, but is not relieved by rest.
Limitation of movement of the lumbar spine in both the sagital and frontal planes.
Limitation of chest expansion relative to normal values correlated for age and sex.
Radiological criterion: Sacrolitis grade>=2 bilaterally or grade 3-4 unilaterally
178
Features of Axial Spondyloarthritis (axSpA)
```
Type of inflammatory back pain.
Enthesitis and dactylitis
Axial involvement
New bone formation/Ankylosis
Extra-articular manifestations *Heterogeneity*
```
179
ASAS classification criteria for axial SpA
In patients with >= 3 months back pain and age at onset <45 years
Sacroilitis on imaging (active (acute inflam on MRI) plus >=1 SpA feature - e.g. inflam back pain, arthritis, enthesis, uveitis, datylitis, psoarsis, IBD, family histoy, elevated CRP
OR
HLA-B27 plus >=2 other SpA features
180
Who gets axSpA and AS?
Onset <45 years
Many in late teens-early childhood 15-35 years
AS = mainly male
axSpA = approaching 1:1 gender split
181
Sympotms in axSpA
```
Inflammatory back pain
Fatigue
Arthritis in other joints e.g. hip, knee
Enthesitis: Achilles tendon, plantar fasciitis
Inflam outside joints = extra-articular:
- Eye: Uveitis
- Skin: Psoiasis
- Bowel - Crohns/UC
- Other: heart, lungs, osteoporosis
Family history of above
```
182
Recommended imaging for axSpA
x-rays = pelvis AP films
Lumbar spin films
MRI allows earlier identification of sacro-ilitits
183
Diagnosis of AS and axSpA
Remains a clinical diagnosis
- suggestive symptoms (inc IBP)
- Imaging
- Associated features e.g. family history, psoriasis, colitis, uveitis
Other investigations:
HLA-B27 status
CRP/ESR (usually normal)
184
Treatment options for axSpA
-
185
Clinical presentation of OA
Joint pain and stiffness
Joint swelling and decreased range of movement
Bouchards nodes - middle finger joint
Heberdens nodes - DCP joints
186
Causes of OA
Previous injury
Abnormal anatomy
Obesity
Jobs with high stress on joint/sports
187
Pathophysiology of OA
Proteolytic breakdown of the cartilage matrix from an increased production of enzymes, e.g. metalloproteinases.
The proteoglycan and collagen fragments released into the synovial fluid as the disease progresses, Erosion to the cartilage roughens the surface and fibrillation which narrows the joint space.
There is increased production of synovial metalloproteinases, cytokines and TNF that can diffuse back into the cartilage to destroy the soft tissue around the knee.
188
Diagnosis of OA
- General examination
- Imaging
```
General examination - include gait
Systemic examination
Specific joint examination
Look/feel/move/special tests
Neurovascular status distally
Leg length measurement
```
Imaging - x-ray will show loss of joint space
Blood
Urine
Aspirate
189
Kellgren Lawrence Stages of OA on radiographs
Stage 0 - no radiographic evidence of OA is present
Stage 1 - doubtful JSN and possible osteophytic lipping
Stage 2 - definite osteophytes and possible JSN on anteroposterior weight-bearing radiograph
Stage 3 - multiple osteophytes, definite JSN, sclerosis, possible bone deformity
Stage 4 - large osteophytes, marked JSN, severe sclerosis and definite joint deformity
190
Management of OA at different stages
Stage 1: Lifestyle - e.g. regular exercise, weight loss
Stage 2: Physiotherapy, strict regimen of exercise and strength training for inc joint stability and weight loss, analgesia as required
Stage 3: NSAIDs, paracetamol or stronger pain-reliefs e.g. codeine, oxycodone; acupuncture, head/cold therapy, massage, local anti-inflam gels; Intra-articular injections of steroid/hyaluronic acid into the joint.
Stage 4: If do not respond to analgesia, physical therapy, weight loss, use of NSAIDs, brace, acupuncture, heat/cold therapy the surgery may be required:
Realignment
Replacement - most common
Excision
Fusion
191
Joint replacement
-
192
Features of juvenile idiopathic arthritis
This is a disease of childhood onset, characterised primarily by arthritis persisting for at least weeks and currently having no known cause
Chronic inflammatory arthropathy, commonest rheumatic disease in childhood
193
Diagnosis of JIA
```
Clinical diagnosis but following tests should be considered:
Acute phase response
Anaemia
ANA
RF
X-rays
```
194
Differential diagnosis of swollen joint in a child
Trauma
Inflammation - infection or autoimmune
Malignancy - leukaemia, bone tumours
195
Know similarities and difference between types of chronic inflammatory arthritis in children compared to adults
-
196
Recognise the key clinical presentations of arthritis in children and how these differ from adults
Clinical signs which occur in children over adults include:
Oligoarthritis
Uveitis
Systemic dises occurs in systemic JIA - fever, rash
Micrognathia occurs in polyarthritis
197
Understand the differences between seropositive and seronegative arthritis
Seropositive:
Symmetrical
Affects small and large joints, often widespread
Commonly affects wrists and MCPS
Seronegative:
Asymmetrical
AS/ERA/Reactive/IBD after lower limb weight-bearing joints
Psoriatic affects large and small joints
