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Rheumatology Revision
Everything you need to know in one hour!
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Likely exam situations
Rheumatology History Hand examination (knee, ankle and foot) Common Rheumatology referrals Back pain- prevalence, approach to Ix and Mx, differentiating inflammatory vs non-inflammatory Connective Tissue Diseases Rheumatology Emergencies- septic joint, vasculitis, lupus flare.
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A quick reminder of joint names
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History taking Presenting Complaint Pain - SOCRATES Arthritis
Inflammatory or non-inflammatory Redness, heat, swelling, early morning stiffness Symmetrical or asymmetrical Mono/oligo/polyarthritis
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Associated features RA: Raynaud’s, fever, malaise, chest symptoms, dry eyes and mouth Seronegative: red sore eyes, back pain, rash, diarrhoea CTD: same as RA + consider alopecia, muscle pain/weakness, difficulty swallowing, rash
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Osteoporosis risk factors
Fibromyalgia Sleep pattern Associated conditions – IBS, migraine
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PMH DH Any arthritic conditions
Any autoimmune conditions (thyroid disease most common) Inflammatory bowel disease Psoriasis DH In a patient with a known diagnosis of inflammatory arthritis, take a full DMARD hx Think about diuretics and antihypertensives if suspecting gout
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FH SH Same as for PMH Maternal hip fracture for osteoporosis
Cigarettes and alcohol Functional status at home and at work System Enquiry
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Joint pain Arthritis Inflammatory Arthritis Non inflammatory Arthritis
Metabolic Vitamin D Paget’s Osteoporosis Soft Tissue Rheumatism Fibromyalgia Regional Pain syndromes
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Fibromyalgia Middle aged women Widespread myalgias and arthralgias
Trigger points Associated sleep disturbance
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Also associated with… IBS Migraine Depression and anxiety Chronic fatigue syndrome (part of a spectrum) A DIAGNOSIS OF EXCLUSION!
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Osteoarthritis Classification Risk factors By site By cause
By features Risk factors Obesity, sex, genetics, hypermobility Trauma, inflammation, sepsis, AVN, slipped epiphysis, obesity, occupation
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Osteoarthritis – clinical features
Hand Heberden’s (DIPJ) and Bouchard’s (PIPJ) nodes 1st CMC squaring Generalised wasting Knee: Quadriceps wasting Crepitus Cool effusion Valgus/varus deformity Instability Hip: Reduced rotation (internal) Trendelenburg +
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X-ray of the knees in a patient with advance OA. Typical features are :
narrowing of the joint space sclerosis (areas of increased whiteness seen especially in the right knee) sub chondral cysts bony overgrowth (osteophytes) degeneration of the articular surfaces Likely symptoms : pain on walking stiffness getting up after walking
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Osteoarthritis – X-rays
Sclerosis Osteophytes Loss of joint space Cysts
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Osteoarthritis - treatment
Lifestyle modification (weight, exercise) Footwear Physiotherapy Quadriceps exercises Occupational therapy Complementary therapies Intra-articular steroid Drugs Simple analgesia NSAIDs – be aware of side effects COX-2 inhibitors – controversy about cardiovascular side- effects Glucosamine – controversy whether it works. Great placebo effect!
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Which of the following statements regarding rheumatoid arthritis is correct?
A negative anti CCP antibody confers a worse prognosis Rheumatoid nodules only occur in seropositive disease Men are affected more frequently than women 1 in 1000 of the population are affected Prednisolone is the first line therapy
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Rheumatoid Arthritis Symmetrical inflammatory polyarthritis
Propensity to affect small joints +ve rheumatoid factor (80-90%) Rheumatoid nodules 1% of adult population Female to male 3:1 Peak onset age 35-45
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Chronic Inflammation in the Rheumatoid Synovium
Activated T cells Pannus Macrophage PMN B cell Cytokine Inflamed synovial membrane Bone Eroding cartilage
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RA – extra-articular problems
Raynaud’s Sicca syndrome Pericarditis Pleuritis/ Pulmonary Fibrosis Subcutaneous Nodules Ocular Inflammation Neuropathies Vasculitis Increased cardiovascular risk
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Goals of Therapy in RA Induce remission Reduce pain and inflammation
Improve physical function Retard/halt joint destruction Improve survival During just the last few years, we have learned how to treat RA better, with the patient-oriented goals of relieving symptoms, preventing joint destruction, improving and preserving the quality of life, and, ideally, achieving clinical remission if not actual cure. To this end, the current generation of biologics have been instrumental in reducing pain and inflammation, improving physical function, and retarding and sometimes even halting joint destruction. Thus, these newer DMARDs hold the promise of improving the quality of life and survival. In 2002, we can’t promise much in the way of remissions. Remissions are rare: Spontaneous = rare DMARD-induced = rare Combo DMARD use = induced remissions on few occasions We need surrogate markers for connection between S&S and radiographic destruction. Primer on the Rheumatic Diseases. 12th ed. Atlanta, Ga: The Arthritis Foundation; 2001:
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RA - treatment Physiotherapy Occupational therapy DMARDs
Methotrexate Sulfasalazine Gold Anti TNF drugs Etanercept Adalimumab Certolizomab B cell inhibitors T cell co stimulator inhibitors IL6 inhibitors
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RA hands 1 Look Typical rheumatoid deformities
Joint swelling,subluxation, swan neck, Boutonniere’s, ulnar deviation Muscle wasting Rheumatoid nodules (remember elbows) Rash Palmar erythema Purpura (and skin thinning) 2ndary to steroids Livedo reticularis / skin mottling (associated with Raynaud’s) Nailfold infarcts / splinter haemorrhages (rheumatoid vasculitis)
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RA hands 2 Feel Move Other bits Is the arthritis active?
Assess function Grip strength Writing Buttons Other bits Consider further muscle and neurological assessment
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OA hands Look Heberden’s nodes Bouchard’s nodes
Squaring of hand (OA of 1st CMCJ) Check elbows (you shouldn’t see anything!) Feel Is there active inflammation? Move Assess function
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Your final statement Come up with a diagnosis
Explain how you got to the diagnosis Comment on function
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Seronegative inflammatory arthritis
Asymmetrical inflammatory oligoarthritis Tends to affect large joints HLA B27 +ve Distinctive features Sacroiliitis Dactylitis Uveitis
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Sero –ve subtypes (RAPE)
Reactive Post infection, esp diarrhoea or STD Reiter’s classic triad of arthritis, urethritis and uveitis Ankylosing spondylitis Classically young men with inflammatory back pain Can also get peripheral arthritis
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RAPE continued Psoriatic arthritis
Can develop before onset of psoriasis 5 different patterns (oligoarticular, RA-like, sacroiliitis, DIPJ and nail involvement only, arthritis mutilans) Enteropathic arthritides Associated with inflammatory bowel disease
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Crystal Arthritides Gout
Inflammatory response to monosodium urate monohydrate crystals (needle shaped, negatively birefringent) Associations: age, sex, alcohol, hypertension, renal impairment, diuretics
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Acute Chronic Rapid onset 90% monoarticular
1st MTPJ in >50% of first attacks Usually settles within 7-10 days Chronic Gouty tophi Urate nephropathy
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Urate Gout. High resolution (3000x) digital videomicroscopy allows a clear visualization of crystal phagocytosis Strongly negatively birefringent under polarised light Measure serum urate
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More crystal arthritides
Pseudogout Calcium pyrophosphate crystal deposition in joints (rhomboid positively birefringent) Mainly elderly, F>M, ubiquitous Acute self-limiting synovitis Chronic arthropathy strong assoc / overlap with OA
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Pyrophosphate
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Septic Arthritis Predisposing factors immunosuppression
pre-existing joint damage iv drug abusers age indwelling catheters 80% monoarthritis, 20% oligo or polyarthritis S. aureus, gram –ve organisms, Neisseria gonorrhoeae
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Connective Tissue Diseases
Rheumatoid arthritis SLE Sjogren’s Scleroderma Polymyositis Dermatomyositis Polyarteritis Nodosa Wegener’s Granulomatosis
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Connective tissue diseases
Common factors Raynaud’s General malaise ANA +ve Raised inflammatory markers Secondary Sjögren’s Lung fibrosis
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Autoantibodies RA Rheumatoid factor SLE
ANA, dsDNA, antiphospholipid antibodies (anticardiolipin, lupus anticoagulant) SSc Anticentromere antibody (limited) Scl-70 (diffuse) Myositis Anti-Jo-1 Wegener’s ANCA Sjogren’s Anti-Ro, Anti-La (part of ENA) Overlap syndromes Anti-RNP (part of ENA)
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Young women Blacks and Hispanics 12/100,000 in UK
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SLE – diagnostic criteria
4 out of 11 of: Malar rash Discoid rash Photosensitivity Oral ulcers Arthritis Serositis (pleurisy, pericarditis, peritonitis) Renal proteinuria >0.5g/24h or 3+ cellular casts Neurological Seizures or psychosis Haematological Haemolytic anaemia or low WCC (<4), low lymphocytes (<1.5) or low plt (<100) (at least x 2 each) Immunological LE cells, or dsDNA, or anti-Sm or false positive VDRL ANA
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SLE – other features Fever General malaise and fatigue Weight loss
Alopecia Other organ involvement Lungs (pneumonitis, pulmonary hypertension) Heart (myocarditis, endocarditis)
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Ix Complete blood count and differential
Comprehensive metabolic profile Creatine kinase Erythrocyte sedimentation rate and/or C reactive protein Urinalysis Quantitation of proteinuria or protein/creatinine ratios
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Autoantibodies in SLE ANA dsDNA Anti Smith (Sm) LA, ACL C3/C4
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Systemic sclerosis Raynaud’s GI problems Lung fibrosis
Oesophageal dysmotility Small bowel overgrowth Bowel failure Lung fibrosis Primary pulmonary hypertension Scleroderma renal crisis
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Limited Systemic Sclerosis
Calcinosis Raynaud’s Esophageal dysmotility Sclerodactyly Telangiectasia
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Hand Exam SSc Look Feel Skin thickening Sclerodactyly Telangiectasia
Calcinosis Ulceration Digital pitting Note any facial features of scleroderma Feel Degree Extent (limited or diffuse disease)
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Gottron’s papules
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Polymyositis and Dermatomyositis
Inflammatory diseases of muscles +/- skin. PM – muscle involvement only DM – heliotrope rash, Gottron’s papules Adults and children, 2-9 cases/million/ year Association with malignancy 20% of DM, 13% of PM Ix – EMG, MRI, muscle Bx
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Vasculitides Small Medium Large Rheumatoid vasculitis - RhF
Henoch-Schonlein purpura – rash, arthralgia, abdo pain Wegener’s granulomatosis – ANCA – kidneys and lun Medium Polyarteritis nodosa Large Temporal arteritis – overlap with polymyalgia rheumatica Takayasu’s arteritis
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A 68 year old woman presents with a 6 day history of headaches
A 68 year old woman presents with a 6 day history of headaches. She describes discomfort when she combs her hair. She has also been struggling to get dressed in the morning. There is no muscular weakness. Blood tests reveal an ESR of 90mm/hr, elevated alkaline phosphatase and a normal CK. What is the most appropriate initial management? Urgent CT Brain Temporal artery biopsy Prednisolone 15mg daily Prednisolone 60mg daily Analgesia and referral to an ophthalmologist
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Approach to temporal arteritis
Refer Urgently but don’t delay treatment Biopsy within 1-2 weeks Start Prednisolone immediately 40-60 mg in uncomplicated disease IV Methylprednisolone in complicated disease Bone Protection , Aspirin Follow up with rheumatologist/GP with protocol for reducing steroids. BSR Guidelines Apr 2010 Uncomplicated GCA (No jaw or tongue claudication or visual symptoms): . Prednisolone 4060mg (not <0.75 mg/kg) daily until resolution of symptoms and laboratory abnormalities [26, 27]. Complicated GCA: . Evolving visual loss or history of amaurosis fugax: i.v. methylprednisolone 500mg to 1 g daily for 3 days [28, 29]. . Established vision loss—at least 60mg prednisolone daily [30, 31]. Bone protection
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The Eye in Rheumatic Disease
Iritis HLA associated / vasculitis Scleritis RA very painful Episcleritis more of a nuisance
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Good Luck!
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If there’s time… Feet Knees Shoulders
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Feet
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Knees
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Vitamin D is a multifunctional prohormone1
The vitamin D endocrine system plays an essential role in calcium homeostasis and bone metabolism, but research during the past two decades has revealed a diverse range of biological actions that include induction of cell differentiation, inhibition of cell growth, immunomodulation, and control of other hormonal systems.1 Vitamin D itself is a prohormone that is metabolically converted to the active metabolite, 1,25-dihydroxyvitamin D [1,25(OH)2D].1 This vitamin D hormone activates its cellular receptor (vitamin D receptor or VDR), which alters the transcription rates of target genes responsible for the biological responses.1 Emerging evidence using mice lacking the VDR and/or 1-hydroxylase indicates both 1,25(OH)2D3-dependent and -independent actions of the VDR as well as VDR-dependent and -independent actions of 1,25(OH)2D3.1 Thus the vitamin D system may involve more than a single receptor and ligand.1 The presence of 1-hydroxylase in many target cells indicates autocrine/paracrine functions for 1,25(OH)2D3 in the control of cell proliferation and differentiation.1 This local production of 1,25(OH)2D3 is dependent on circulating precursor levels, providing a potential explanation for the association of vitamin D deficiency with various cancers and autoimmune diseases.1 Vitamin D is important for MSK health, immune system and CVS system. Adapted from Dusso AS et al. Am J Physiol Renal Physiol 2005; 298(1): F8-28.
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Effects of Vitamin D deficiency
Reduced calcium gut absorption Reduced serum calcium Increased PTH Secondary hyperparathyroidism Phosphaturia Calcium bone resorption Bone demineralization
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Identifying adults at risk of vitamin D deficiency in clinical practice
Adult at risk groups1 People over 65 years of age Thinning of the skin reduces the efficiency of vitamin D synthesis Inadequate sunlight exposure Covered skin for medical, social, cultural or religious reasons, housebound Non-whites Darker skin pigments interfere with UV light reaching the appropriate skin layer Poor health Low HDL, no daily milk Obesity Possibly related to unbalanced diet, low HDLs. Adult groups at risk of vitamin D deficiency include:1 Older people, aged 65 years and over People who have low or no exposure to the sun, for example those who cover their skin for cultural reasons, who are housebound or who are confined indoors for long periods People who have darker skin, for example people of African, African- Caribbean or South Asian origin, because their bodies are not able to make as much vitamin D. Skin synthesis of vitamin D is negatively influenced by factors which may reduce the ability of the skin to provide the total needs of the individual: Latitude and season: both influence the amount of UV light reaching the skin The ageing process: thinning of the skin reduces the efficiency of this synthetic process Skin pigmentation: the presence in the skin of darker pigments interferes with UV light reaching the appropriate layer of skin Clothing: virtually complete covering of the skin for medical, social, cultural or religious reasons leaves insufficient skin exposed to sunlight Sunscreen use: widespread and liberal use of sun-blockers reduces skin damage by the sun but also deleteriously affects synthesis of vitamin D. National Osteoporosis Society Practical Guidelines. Vitamin D and Bone Health: A Practical Clinical Guideline for Patient Management. April Available at: NHANES Survey
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Manifestations and symptoms of vitamin D deficiency1
Osteomalacia in adults Rickets in children Insufficiency Secondary hyperparathyroidism Bone loss Muscle weakness Falls and fragility fractures in older people Symptoms Bone pain (ostealgia) Joint pain (arthralgia) Muscle pain (myalgia) Muscle weakness Difficulty walking Fractures National Osteoporosis Society Practical Guidelines. Vitamin D and Bone Health: A Practical Clinical Guideline for Patient Management. April Available at:
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