RHEUMATOLOGY.

RHEUMATOLOGY

Rheumatoid arthritis Fibromyalgia Osteoporosis Ankylosing spondylosis Juvenile Idiopathic arthritis Reactive Arthritis Gout, Pseudogout Misc

RHEUMATOID ARTHRITIS Maryam Nauman

Loss of job, reduced working hours, off sick, reduced family income
In UK, 26,000 new cases diagnosed per year, More than 690,000 cases already living with this condition ECONOMIC IMPACT Loss of job, reduced working hours, off sick, reduced family income Annual impact of RA in Western Europe 42 billion Euros RA costs £8 billion/year to UK economy

37 Year old presents to you with pain in joints very suggestive of Rheumatoid arthritis
Asymmetric arthritis more than 6 weeks duration Absence of soft tissue swelling Morning stiffness more of than 1 hour duration for at least 6 weeks duration Normal X-rays

DIAGNOSIS-ACR Criteria
• AM STIFFNESS (1 h) • INFLAMMATORY ARTHRITIS OF ≥ 3 JT AREAS • INFLAMM ARTHRITIS OF HAND JTS (wrist MCP PIP) • SYMMETRIC ARTHRITIS • RHEUMATOID NODULES • SERUM RHEUMATOID FACTOR OR ANTI-CCP • RADIOGRAPHIC CHANGES TYPICAL OF RA FOR ≥ 6 WKS Any 4 = rheumatoid arthritis Specificity: 40-60%, %

Classification criteria for RA (score-based algorithm: a score of ≥6/10 is needed for classification of a patient as having definite RA) Joint involvement 1 large joint- 0, large joints-1 1-3 small joints (with or without involvement of large joints) -2 4-10 small joints (with or without involvement of large joints) -3 >10 joints (at least 1 small joint)- 5 Serology (at least 1 test result is needed for classification) Negative RF and negative ACPA-0 Low-positive RF or low-positive ACPA-2 High-positive RF or high-positive ACPA-3 Acute-phase reactants (at least 1 test result is needed for classification) Normal CRP and normal ESR-0 Abnormal CRP or abnormal ESR-1 Duration of symptoms <6 weeks- 0 ≥6 weeks-1

Who would you refer to specialist
37 year old female with pain effecting small joints of both hands 54 year man old with pain and tenderness in hip joint 35 year old female with fever, generalised tiredness and increased CRP and positive RF

Referral for specialist opinion
Any person with suspected persistent synovitis of undetermined cause REFER URGENTLY IF ANY OF THESE ARE AFFECTED Small joints of hands or feet are affected More than one joint is affected There has been a delay of 3 months or longer between onset of symptoms and seekin medical advice

PHARMACOLOGICAL MANAGEMENT
INVERTED PYRAMID NSAIDS, ANALGESICS – For pt who may not have RA – To ease pain while waiting for the 6 week point for spontaneous improvement • DMARD – In any patient with RA without contraindication – Methotrexate, hydroxychloroquine, sulfasalazine – leflunomide • MORE THAN ONE DMARD: 3>2 = biologic; 2>1 – If you do not want to give biologic – cost, toxicities • BIOLOGIC AGENT PLUS METHOTREXATE – For any patient without excellent response to DMARD

DMARD DRUG DOSE SIDE EFFECTS MONITORING REQUIREMENTS SULFASALAZINE
Oral 500 mg upto 3g/day Nausea, rash, neutropenia, low sperm count, abnormal LFT FBC, LFT at start, FBC 2 weekly, LFT 4 weekly for 12 wks, 3monthly for yr then 6 monthly METHOTREXATE Oral 7.5 g/wk upto 20mg/wk,add folic acid 5mg 3days after each dose Alopecia,rash, N, D, fhepatic fibrosis,leucopenia, mouth ulcer FBC, UE,LFT,CXR baseline. FBC weekly until 6wks afterlast dose increase,then monthly LFT LEFLUNOMIDE Oral loadin dose 100mg,,maintenanc10-20 m Diarrhea,rash,hair loss, HTN, nausea, increased liver enzymes FBC basline,every 3 weeks for 6 months then every 8 weeks, ALT baseline and then monthly~6m, monitor BP

HYDROXYCHLOROQUINE Oral 200 mg Rash, GI upset, retinl al toxicity Basleine ophthalmo, then 6 monthly, and annualy Penicillamine-obsolete Oral 125m/day Rash, nausea,loss of taste,pancytopenia, proteinuria Basline FBC,UE,urinalysois, then monthly Sodium aurothiomalate- now obssolete I/M 10 Rashm mouth ulver,proteinuriaa, pancytopenia, nephrotoxicity FBC, urinalysis baseline and before each injection AZATHIOPRINE 1.5-3 mg/kg/day Bm supp, GI upset, ,hepatitis FBC baslein and monthly

ANTI-TNF THERAPY @-TNF Inhibitors- active arthritis, have undergone trial of 2 DMARDS inc methotrexate Infliximab-IV infusion Etanercept- in children also-s/c injections Adalimumab-s/c inj Anti IL1-Kineret,Ticlizumab, Rituximab, Abataccept orencia

Nicolas Milhavy GP ST1 VTS
Fibromyalgia Nicolas Milhavy GP ST1 VTS

Not well understood despite widespread research in the USA, Canada and Europe…… Can have a definite trigger or can come on gradually out of the blue

Diagnosis A history of chronic and widespread pain (CWP)
‘Pain and fatiguability with multiple hyperalgesic tender sites (11/18)’

American College of Rheumatology – Classification (1990)
Pain in the left and right side of the body, pain above and below the waist and axial skeletal pain (shoulder and buttock included on each side and lower back pain considered lower segment pain) for at least 3 months

American College of Rheumatology – Classification (1990)
2. Pain (not tenderness) with digital palpation in 11/18 sites Occiput – bilaterally Low cervical C5-C7 Trapezius – bilateral Supraspinatous – above scapula Second rib – bilateral Lateral epicondyle – bilateral Gluteal – bilateral Greater trochanter – bilateral Knee - bilateral

‘Manchester’ Definition
Pain must be present in 2 separate sections of a body quadrant to be positive

Epidemiology CWP prevalence is above 10% if American College of Rheumatology definition is used CWP prevalence is 5% with ‘Manchester’ definition Twice as high in females Fibromyalgia % in comparable studies using ACR criteria 90% female, peaks aged 40-50

Clinical picture Pain – axial and diffuse, felt all over
Pain worsened by stress, cold and activity, association with EM stiffness Parasthesiae in hands and feet common Analgesics and NSAIDs ineffective and may worsen symptoms Poor sleep pattern – wake exhausted and poor concentration Anxiety and depression scores are high Unexplained headaches, urinary frequency and abdominal symptoms are common Clinical findings unremarkable

Pathogenesis A poor, unrefreshing sleep pattern – unable to enter the 4th phase of sleep (deep refreshing sleep) Muscles do not relax and resting muscle tension is raised – this causes aching all over that means the person cannot sleep well the following night – a vicious circle that is difficult to get out of Napping in the day worsens symptoms as it means the body cannot enter the restorative phase Low levels of NTs in the brain and abnormal processing of sensory stimuli – light touch and movements can cause significant pain that is real with no structural explanation Reduced aerobic fitness Behavioural affective symptoms

Differential Diagnosis
Hypothyroidism SLE Sjorgren’s Psoriatic arthritis Inflammatory myopathy Hyperparathyroidism Osteomalacia

Diagnosis Exclude differential
FBC, ESR, TFTs, U and Es, Calcium, CK, phosphate, ANA, RhF and immunoglobulins

Management Good explanation Avoid unnecessary investigation
To patient and the family Relieve concerns of sinister causes for pain Rationalise with lack of sleep and fitness Avoid unnecessary investigation Regulate a better and more refreshing sleep pattern Increase aerobic exercise or physiotherapy (a graded and sustainable exercise regime) Low dose amitriptylline, dothiepin or fluoxetine Consider CBT or counselling MDT approach with rheumatology and pain clinic

Prognosis Poor 20% are symptom free at 5 years
Treatment may help with coping strategies

Case History Joblu Khan

Mr ARL 54 year old gentleman Difficult patient Well read
Frequent attender ‘Hypochondriac’

Mr ARL “Osteoporosis” “aches and pains all over” Recent wrist fracture

Mr ARL Winter (December) 2010 Fall onto outstretched hand (L hand) ED
999 # wrist L Backslab 6/52 Finger, elbow and shoulder exercises Discharged from ortho recently Dr S Hameed (SHO)

Mr ARL Consultation Risk Stratification

Mr ARL Body weight Nutritional Lifestyle Family history PMH DH
‘chubby’ (BMI 25 to 30) Nutritional Takeaway and microwave meals Lifestyle Enjoys walking the dog Limited knee pain Ex smoker (10 pack year history) 2 cans of Guinness most nights Family history Mother osteoporosis Severe COPD PMH HTN High cholesterol Diabetes Mellitus (diet controlled) Mild OA L knee DH Amldoipine Simvastatin Paracetamol PRN

Mr ARL Bld tests (random) FBC, ESR U&Es LFTs (ALP 154 (40 – 129)) Bone
TSH Testosterone Random glucose (11.2 mmol/L) Cholesterol (4.5 mmol/L)

Mr ARL DEXA scan T score of – 2.6 What is the diagnosis?
Treatment of choice? Need to refer? Follow up investigations needed?

Mr ARL

Osteoporosis Systemic skeletal disease
Low bone mass and micro-architectural deterioration Increase in bone fragility and susceptibility to facture Considerable morbidity and mortality Increasing in developing countries Increasingly elderly population

Investigate Previous low trauma fractures # from fall from standing
Loss of height/kyphosis (? Vertebral #) Age > 60 and female sex Recurrent falls Glucocorticoid use FH of osteoporosis Secondary causes

Diagnostic evaluation
Degree of osteopenia DEXA Establish current fracture risk Establish future fracture risk Monitor effect of treatment Osteopenia Tscore – 1 and – 2.5 Osteoporosis T score <2.5

Diagnostic evaluation
Exclude secondary osteoporosis Primary hypoparathyroidism (serum Ca) Thyrotoxicosis (TSH) Myeloma (ESR, plasma electrophoresis, BJ proteins) Osteomalacia (serum Ca, Phosphate, ALP) Malabsorption syndrome (FBC) Hypogonadism in men (testosterone)

Management Anti resorptive drugs Etidronate Alendronate Risedronate
Didronel® Alendronate Risedronate Ibandronate Raloxifene SERM HRT Testosterone therapy Hypogonadism Calcitonin Calcium and Vit D Calcichew D3 forte

Management Formation stimulating drugs Treating secondary causes
Recombinant fragment of parathyriod hormone Specialist centres Strontium ranelate Treating secondary causes Partial recovery Preventing falls Predisposing causes Postural hypotension Physiotherapy Hip protectors

Preventing osteoporosis
Optimize peak bone mass Exercise Regular and weight bearing Dietary calcium Reduce rate of bone loss HRT Calcium intake Moderate alcohol intake Stop smoking Prophylactic treatment ? Cost effectiveness

Osteoporosis Determine risk Preventable Treatment effective
? Guidelines QOF?

Case Presentation Ulfat Younis

32 year old Male Works as a Brick Layer
Lower Back Pain Comes and goes Persistent episodes past few years Worse at night (wakes from sleep) and at rest Better with Exercise Stiffness, better through the day Associated Lethargy and low mood Has had 2 episodes of painful and red eye over last 12 mnths... What More Do You Want To Know? What is the likely Diagnosis?

Ankylosing Spondylosis
Ankylosis= Fusion across a joint Spondylosis= Inflammation Sacroiliac and Vertebral joints Affects Young Males (Age 20-40Yrs), 3-5x>more common in Men. Anterior Uveitis (40%), Other Tendon/Joint involvement Unknown Aetiology Hereditary Tendency HLA-B27 (9/10 with AS are +ve)

Diagnosis History: Persistent, grumbling episodes of Back pain and Index of suspicion. Differentiate from ‘Mechanical Back Pain’. Investigations: Bloods Inflammatory Markers in acute phase X ray Sacroiliitis,‘Bamboo spine’ fusion, Delayed changes MRI Earlier changes, inflammation of SIJ

Treatment Ease Pain, reduce stiffness, maintain mobility
Physiotherapy + NSAIDS for flare ups Immunosuppressant Drugs: Biological Therapies TNF-Alpha Blockers Monoclonal AB (Etanercept, Infliximab) NICE: Adalimumab/Etanercept for severe AS + Active spinal disease (assessed 2x 12 weeks apart Have tried at least 2 NSAIDs ineffectively Immunomodulators Suppression of the immune response (Sulphasalazine) ?Effectiveness in AS

Prognosis Good..intermittent flare ups, mild-moderate severity Regular exercise (Low impact)+ Analgesia to control symptoms Gradually increasing stiffness with age 8/10 remain fully independent with limited disability (despite eventual spinal restriction) 1/10 severe form AS...Anti-TNF Rx promising Extra-axial: Lung Fibrosis Restrictive defects, Parasthesia, Amyloidosis, AR, Enthesopathy etc..

Juvenile Idiopathic Arthritis
Gordon irvine

Case Study 15 year old boy School sports star (captain of rugby)
Developed swollen fingers and knees Lumps on back of wrists Otherwise well No Fam Hx

JIA Any arthritis-related condition < 18yrs
1 in 1000 children in UK Most types more common in females Most children won’t have lasting impact

Oligoarthritis Most common (60%) Girls < 5yrs Mildest
1-4 joint in first 6mths (knee, ankle, wrist) Morning stiffness Moodiness Walking? Uveitis (1in 5)

Polyarthritis 2nd most common 20% (girls>boys) 5 or more joints
Hands and feet > knees, wrist, elbows, ankles, hips, neck, jaw Soreness of tendons of hands Unwell +/- fever

Systemic Arthritis (Still’s Disease)
10% (boys=girls) often aged <5 Affects body as whole Difficult to diagnose ? Pericardium Fever lasting several weeks and rash

Psoriatic Arthritis Associated with psoriasis Girls 8-9 yrs
? Uveitis ? Pre dates psoriasis

Enthesitis-related Arthritis
Usually affects boys > 8yrs Arthritis in several joints (sacroiliacs and tendon insertions) Eyes often affected Associated with HLA-B27

What Causes JIA? No clear evidence passed down through families.
Certain illnesses may act as trigger on those with genetic predisposition

Diagnosis Bloods: FBC, ESR, CRP, U&E, LFTs, Autoantibodies
Xrays and USS/MRI Eye Tests

Treatment Referral Drugs (NSAIDs, DMARDS, Steroids, Biologics, Eye Drops) Physiotherapy Surgery

Self Help Exercise (encourage) Diet (Calcium, Vit D and Iron)
Pain Management Others (Complementaries, aids etc)

Where’s our case? 32 yrs old married
Lived in Boulder, Colorado for 7 years Summer: climbing, mountain biking and outdoor guide Winter: ski instructor and guide

Can’t pee, can’t see, can’t climb a tree!
Kathryn Burnett

Reactive arthritis Sterile inflammatory oligoarticular arthritis occuring 2-4 weeks following a remote infection Usually following urogenital or enteric infection Most patients aged 20-40 Asymmetrical lower extremity oligoarthritis 75% are HLA B27 positive. Seronegative spondyloarthropathy. 10% of patients do not have preceeding infection

Prognosis 25-50% of patients will have further acute episodes of arthritis 15% proceed to chronic arthritis (more likely if HLA B27 positive) requiring referal to rheumatology for consideration of DMARDs Most patients symptoms resolve within 3-12months 1 In 100 patients with urethritis will develop reactive arthritis

Remember STI screen for young person presenting with oligoarthritis even if no urogenital symptoms.

GOUT & PSEUDOGOUT Jennifer Thornhill

Answers Colchicine Intra-articular steroid injection IM steroid
Methotrexate Oral steroids Physiotherapy Probenecid Referral for surgery Rest Splinting

De Qervain’s tenosynovitis not responding to rest and a wrist support
Early morning stiffness and pain in shoulders with raised ESR Acutely swollen first MTP joint Acute onset lumbar backakce when lifting with right sided sciatica Pt with fibromyalgia complains of multiple tender points in her shoulders; examination reveals normal range of movement but numerous trigger points within the muscles.

Case SH: drinks 15 pints per week. 42 year old male police officer
Acutely swollen, hot right knee Feels tight, limping slightly No history injury PMH: prev ACL repair, previous patellar dislocation, high cholesterol, gout (toe and thumb – once a year for 8 years) SH: drinks 15 pints per week.

Examination Moderate effusion to knee Warm to touch No erythema
Ligaments stable Recent exacerbation gout in right thumb – improved with indometacin. Been taking last 3d for knee – no improvement.

Differentials Infection Rheumatoid arthritis Bunion
cellulitis septic bursitis aseptic arthritis Rheumatoid arthritis polyarticular gout that affects the fingers may be mistaken for rheumatoid arthritis if there are elbow tophi these may be mistaken for rheumatoid nodules Bunion Chondrocalcinosis - pseudogout Seronegative arthritis

Investigations Serum urate (optimal time 2w after attack)
Leucocytosis and raised ESR/CRP during attack Assess other CV risk factors – fasting lipid, BP, glucose Aspiration and polarised light microscopy of synovial fluid Radiology

Treatment Correct exacerbating factors
Consider stopping or reducing diuretics Reconsider aspirin Reduce alcohol intake Reduce intake of purine rich foods NSAIDs – 1st line = indometacin, diclofenac, naproxen Azapropazone Etoricoxib 120mg daily

Treatment alternatives
Colchicine in patients with peptic ulcer disease / heart failure / CIs to NSAIDs / HTN can be combined with anticoagulation does not cause fluid retention Dose is 1 mg, then 500 mcg every 2-3 hours until the pain resolves, or the patient develops diarrhoea, or a total dose of 6mg has been taken. Treatment with colchicine should not be repeated within 3 days. Common side effects are diarrhoea and gastric irritation. Steroids – tapering oral dose / IM injection / intra-articular (large joint)

If not subsiding in 12-24h, reconsider diagnosis

Gout Disorder of purine metabolism
Characterized by acute, recurrent attacks of synovitis due to urate crystal deposition Leads to cartilage degeneration Most common in men (20:1) and in post-menopausal women

Primary (95%) – inherited discorder that causes overproduction/underexcretion. Underlying biochem defect unknown Secondary Increased formation uric acid Reduced excretion Drugs/toxins Misc

The great toe demonstrates extensive juxta-articular erosions with soft tissue swelling and little osteoporosis

Chronic gout Frequent recurrence of acute attacks of gout, the presence of tophi, or signs of chronic gouty arthritis may call for the initiation of long-term (‘interval’) treatment 2 choices: xanthine-oxidase inhibitors uricosuric drug – sulfinpyrazone, probenecid, benzbromarone

Allopurinol Xanthane oxidase inhibitor Reduces synthesis of uric acid
Can precipitate an attack - give NSAID/colchicine concomitantly for first 3 months Do not commence during acute attack – can prolong. Start 1-2 weeks later. Can cause rashes

Febuxostat Licensed for the treatment of chronic hyperuricaemia where urate deposition has already occurred 80mg once daily for patients who are intolerant of allopurinol or for whom allopurinol is contra-indicated

Gout vs. pseudogout Gout Pseudogout Age Patients tend to be over 40
Elderly Sites affected Small joints Large joints (most commonly the knee) Clinical features Severe joint pain & swelling Moderate joint pain & swelling Radiological features Soft tissue swelling (not seen until 6-12 yrs after initial attack) Chondrocalcinosis calcification of articular cartilage menisci Crystal deposition Uric acid Calcium pyrophosphate Treatment Rest, NSAIDs, ?allopurinol Rest NSAIDs, joint aspiration

Pseudogout associations
hyperparathyroidism haemochromotosis diabetes mellitus Wilson's disease ochronosis hypophosphataemia oxalosis osteoarthritis gout dialysis long-term steroid therapy acromegaly

MISC Sukhvans Sandhu

Case 1 A 26 yr old woman c/o painful blue discolouration of her fingers on exposure to cold temperatures. She recalls having such episodes as a child but noted that they became more frequent when she moved to the coast. On recent outdoor walks she has felt increasing pain in her fingers and watched as they turned white, then blue, and finally became red and swollen. Once her hands were warm again they returned to normal. On examination nil significant.

Raynauds Pathogenesis: Exaggerated vasoconstriction of arteries and arterioles [usually hand and feet] Causes: Mostly idiopathic, cold, emotions

Raynauds cont. Symptoms:- Pain within the affected extremities
Discolouration [white, blue, red] Sensation of cold and numbness Prevalence More common in women than men

Primary Raynauds Primary Raynauds disease:-
Reflects exaggeration of central and local vasomotor responses to cold or emotional stresses. Course of Raynauds is usually benign, however when long-standing can result in:- Atrophy of the skin, subcutaneous tissue and muscles Ulceration and ischaemic gangrene [rare]

Secondary Raynauds Secondary Raynauds
Refers to a vascular insufficiency of the extremitites secondary to arterial disease:- Connective tissue disorders: SLE, sceleroderma [Specific-systemic sclerosis- CREST] Obstructive disorders: Atherosclerosis, Buerger disease Drugs: b-blockers, sulfasalazine Occupation: jobs involving vibration Raynauds may be the first manifestation of such conditions so be ready to consider.

Treatment General care:-
Avoid triggers e.g. cold, vibration, emotional stress Keep hands and feet warm- mittens, insulated foot wear. Quit smoking Avoid caffeine Drug therapy Medicines that dilate blood vessels Calcium channel antagonists [Nifedipine or diltizem] – headache, flushing, ankle oedema Fluoxetine [SSRI] reduce frequency if associated with emotional trigger. Surgical – may require sympathectomy; botox

The most common cause of Raynaud's Phenomenon is. A. Idiopathic B
The most common cause of Raynaud's Phenomenon is? A. Idiopathic B. Rheumatoid arthritis C. Scleroderma D. Systemic Lupus Erythematosus E. Through the use of vibrating tools or machinery

Raynaud's disease is a recognised feature of:- A. Cervical rib B
Raynaud's disease is a recognised feature of:- A. Cervical rib B. Scleroderma C. Buergers disease D. Diabetes mellitus E. SLE

Case 2 A 45yr old woman presents with bilateral painful and deformed DIP joints. She also states that over the past few weeks that her eyes appear red. Further examination reveals discolourisation and onycholysis of the nails.

Psoriatic arthritis Is a type of inflammatory arthritis
Affects around 10-30% of people suffering from the skin condition psoriasis Seronegative spondyloarthropathy App 80% of patients with psoriatic arthritis will have psoriatic nail lesions Can occur at any age Occurs app 10yrs after the first signs of psoriasis Men and women equally affected

Psoriatic arthritis cont.
Presentation:- Causes joint, ligament inflammation Sausage-like swelling of digits [dactylitis] Joint stiffness [worst in morning; resting] Skin rash of psoriasis Pitting of nail

Types of psoriatic arthritis
Asymmetric: 70% of cases. Symmetric: 25% of cases. Affects joints on the same side of the body simultaneously. Arthritis mutilans: <5% of cases. Severe deforming and destructive artritis Spondylitis: Characterised by stiffness of the neck or spine. DIP predominant: 5% of cases. Inflammation and stiffness in the DIP joints.

Treatment Underlying process of psoriatic arthritis is inflammation  control inflammation First line: NSAIDs [ibuprofen, diclofenac] Joint injections [corticosteroids] Second line: If NSAID and/or steroids not working need immunosupressants:- Methotrexate, Leflunomide Adv: immunosupressant treatment [covers arthropathy and psoriasis]. Severe cases: a-TNF agents e.g. inflixamab [reserved for the most severe cases.

Psoriatic arthropathy is associated with which ONE of the following features:-
A. A preceding history of skin lesion in the majority of patients B. Non involvement of the DIP joints C. Subcutaneous nodules D. Gallstone in the majority of patients E. The development of some evidence of joint involvement in the majority of patients with psoriasis

In psoriatic arthropathy:-
A. HLA B27 is associated with spondylitis. B. Arthritis mutilans is the most common pattern C. Onychopathy (nail pitting, ridging or onycholysis) is frequently associated with disease of the adjacent DIP joint. D. The severity and extent of synovitis is proportional to the extent of the psoriasis. E. Sulfasalazine might improve both psoriasis and arthritis.

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