Phase 2 Erin Whyte Jamie McConnell Rheumatology The Peer Teaching Society is not liable for false or...
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Transcript of Phase 2 Erin Whyte Jamie McConnell Rheumatology The Peer Teaching Society is not liable for false or...
Phase 2
Erin WhyteJamie McConnell
Rheumatology
The Peer Teaching Society is not liable for false or misleading information…
The Peer Teaching Society is not liable for false or misleading information…
aims
The Peer Teaching Society is not liable for false or misleading information…
Rheumatological HistoryPatient DemographicsSex, AgeEthnicityHandednessOccupation
JointsGeneral - how many, which (large/small/both/weight-bearing), symmetryPain - SOCRATES, night pain? pain now? rest/movement? analgesia tried?Stiffness - when, where, how long does it last?Swelling - when, where, how long does it last? relation to activity?Deformity - where, for how long, speed of progression?
Associated SymptomsRashes, photosensitivity, psoriasis, changes in skin pigmentation, Raynaud’s phenomenon, alopecia, dry or red eyes, dry mouth, ulcers (oral, nasal, genitals), dysphagia, dyspnoea, loss of sensation/pins and needles, myalgia, muscle weakness, headaches/migraines, cognitive disturbance, depression, seizures, fever, weight loss, change in bowel habit
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Rheumatological History
Additional PointsFlares - frequency, severity (hospitalisation?), what exactly happened and which body part was affected?Functional disability - ADLs eg cooking (opening jars?), dressing (buttons?), overhead activities, walking distances, stairsPrevious treatments - what? duration? effectiveness?
PMHAny condition relating to the presenting complaintPsoriasis, IBD, IBS, hypertension, gout, recurrent infections, trauma, miscarriage, PE, DVT, blood transfusions, tattoos, STIs, travel history, cardiorespiratory conditions, GI conditions, GU conditions, medication history (including OTC, illicit drugs), allergies
Family and Social HistoryArthritis (type, age of onset), IBD, psoriasis, gout, Marfan syndrome, Ehlers-Danlos syndrome, ankylosing spondylitisHome circumstances, type of property, adaptations, co-inhabitants and relationshipSmoking, alcohol (past and present), recent stressful events, ability to relax/sleep, sexual history
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Rheumatological History - inflammatory or not?
Inflammatory symptoms are -• Stiffness Worse in the early morning or after a period of inactivity - progressively easing as the day goes on• Pain present at rest as well as on movement
Examination - • Overlying skin warm and red• Tenderness across the joint line• Swelling• Pain
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Osteoarthritis • 1/4 >65 have symptomatic hip or knee OA, 70% >70 = radiological change• Risk factors - increasing age, female sex (knee), joint injury, obesity, strenuous occupation• Joint pain usually related to use - also stiffness, reduced RoM, deformity and instability• Heberden and Bouchard nodes• Most commonly affected joints = hips, knee, spine, 1st MCPJ, DIP, PIP
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The Peer Teaching Society is not liable for false or misleading information…
Osteoarthritis - x-ray
• Osteophyte• Joint space narrowing• Subchondral Sclerosis• Subchondral Cysts
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Osteoarthritis - managementText
• Patient education and lifestyle measures - weight loss etc• PT, OT• Supportive aids e.g. supports and braces• Paracetamol and topical NSAIDs first line• NSAIDs second line (+PPI)• Opioids• Intra-articular steroids• Surgery - arthroscopy
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Crystal Arthropathy - GoutText
• Male 40-50 years, dietary purine intake, alcohol, diuretics• Classically mono-arthritis (50% 1st MTPJ)• Severe pain, swelling, tenderness (duvet on foot)• Chronic gout - tophi• Uric acid - negatively birefringent needle shaped crystals on aspirate• Acute attack - NSAIDs, colchicine, intra-articular steroids• Prophylaxis - Allopurinal (not during acute attack - prolongs symptoms)
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PseudogoutText
• Calcium pyrophosphate arthropathy• Increasing age, hyperparathydroidism, diabetes, Wilson’s disease, hypothyroidism• Larger joints - acute, hot, swollen, effusion• Positively birefringent rhomboid shaped crystals on aspiration• NSAIDs, IA steroids
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Crystal ArthropathyText
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Rheumatoid Arthritis: Pathophysiology
Rheumatoid arthritis is a chronic, systemic,
inflammatory disease of unknown aetiology that
primarily affects the peripheral joints in a symmetrical pattern
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Rheumatoid Arthritis:Joint involvement
Worldwide prevalence = 1%Peak age of incidence = early 40sWomen>Men (though sex ratio varies with age)Genetic factors - familial aggregation and HLA DR4 association
TMJ 25%
C Spine 35%
Glenohumeral 60%
Elbow 70%
Hip 25%
Knee 80%
Ankle 40%
MTPs 80%
Carpus 80%
MCPs 85%
PIPs 65%
Initially small joints affected asymmetrically, eventually symmetrically followed by involvement of larger joints
Joint swelling, tenderness, pain and stiffness - particularly in the morning, improving as the day goes on
Rheumatoid Arthritis: Extra-articular manifestations
Elbow nodules
Carpal Tunnel Syndrome
Splinter haemorrhage
Splenomegaly (1% Felty’s syndrome = splenomegaly + neutropenia + lymphadenopathy)
Ischaemic ulceration(vasculitis)
Distal symmetrical sensorimotor neuropathy
Nodules on achilles tendon
Renal disease (secondary to drugs and amyloid)
Alveolitis → FibrosisNodulesPleuritisPericardial Effusion
PericarditisNodule in conductive tissue → AV blockNodule on valve → murmur
EpiscleritisScleritisKerato-conjunctivitis sicca
Systemic - fever, anorexia, malaise, weight loss, lethargy
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Rheumatoid Arthritis: Hands
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Rheumatoid Arthritis: Diagnosis Bloods -• ESR •CRP•FBC
Immunology -• RhF - >70%, denotes worse prognosis• anti-CCP (more specific than RhF)
Imaging - • X-rays - SPADESS - soft tissue swellingP - periarticular osteoporosisA - absent osteophytesD - deformityE - erosions - usually within 2 yearsS - subluxation(often only tissue swelling at presentation)• US - early inflammation
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Rheumatoid Arthritis: Management Symptomatic Relief - simple analgesics or NSAIDs (consider PPI)Modification of underlying disease - DMARDs - methotrexate, sulfasalazine, azathrioprine, gold, ciclosporin, antimalarialsAdjunctive therapy with corticosteroids - systemic, into affected joints) Biological agents - persistently active disease despite treatment with at least 2 DMARDs (including methotrexate)
NICE 2009 - DMARDs asap post-diagnosis (avoid further damage), combination therapy including methotrexate + short term steroids (takes up to 3 months for benefits of DMARDs)
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Seronegative spondyloarthropathies
Ankylosing SpondylitisPsoriatic ArthritisReactive ArthritisEnteropathic Arthritis
HLA B27
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Ankylosing Spondylitis
• Onset = late teens/early adulthood (<40)• Men>Women (2.5:1)• Insidious onset of inflammatory type back pain in lower back/buttocks and/or thoracic region
Inflammatory back pain - Young age
Significant early morning stiffness (>20 minutes)Improvement on exercise
Localised tenderness over sacroiliac joints - alternating buttock painPain at night
Responds to anti-inflammatory medication • Extrasketletal manifestations include aortic regurgitation, upper lobe fibrosis and irits/uveitis
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Ankylosing Spondylitis
X-ray findings Fusion of vertebral bodies (‘Ankylosing’) - late stageJuxta-articular sclerosis, erosions, widening of sacroiliac jointsSyndesmophyte formation, ‘bamboo spine’
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Ankylosing Spondylitis - management
•Physiotherapy•NSAIDs•Methotrexate or sulfasalazine - for peripheral joint arthritis (not axial disease)•Anti-TNFα/biologics - severe/persistent •Topical Corticosteroids (uveitis)•Intra-articular steroids
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Psoriatic Arthritis
• Chronic seronegative inflammatory arthritis associated with psoriasis• 10% patients with psoriasis (1.5% UK population) - may develop arthritis prior to psoriasis• Peak age of onset 35-55 years, women>men, western caucasian population• Different patterns of disease - symmetrical polyarthritis (DIP common), asymmetric oligoarthritis, spondylitic pattern, arthritis mutilans, juvenile onset • Additional features - nail changes, ocular invovlement• Differs from RA - RF -ve, anti-CCP -ve, no nodules, less deformity etc
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Psoriasis
Red, silver-scaled lesions - predominately extensor surfaces and scalp
Nails - pitting, yellowing, onycholysis, leukonychia, transverse ridging
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Reactive Arthritis
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Reactive Arthritis
•Sterile arthritis occurring following infection at a distal site•Reiter’s Syndrome (archaic term!) - arthritis, urethritis, conjunctivitis (Can’t see, can’t pee, can’t bend the knee)•Tends to occur 2-4 weeks post-infection, can last several months•Systemic features (including malaise, fatigue, fever)•Ix - Elevated inflammatory markers, RF and ANA -ve, white cells and bacterial antigens on joint aspiration•Mx - Initially rest the joints, then physiotherapy. NSAIDs, steroids (Intra-articular), if causative organism found ?antibiotics, DMARDs if chronic/recurrent
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Enteropathic Arthritis
Arthritis associated with IBD
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Systemic Lupus Erythematous
SLE is a chronic, autoimmune, inflammatory,
multisystem, connective tissue disorder that can
affect almost any system in the body
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SLE - epidemiology
Aetiology unknown - multiple genetic and environmental factors Classically women, age 20-40More common in Afro-Caribbean, Asian and Hispanic communitiesMay be drug induced (men>women - tetracyclines, methyldopa etc)
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SLE - diagnostic criteria
•Malar rash•Photosensitive rash•Discoid rash•Neurological involvement (headaches, especially migraines, psychosis, seizures, depression)•Renal disease (proteinuria, casts)•Serositis (pleuritis, pericarditis)•Mucosal aphthous ulceration•Arthritis•Haematological abnormalities •Immunological abnormalities •ANA positive
4/11 criteria present at any time is required for diagnosis of SLE
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SLE - presentation
Malar Rash
Discoid Rash
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SLE - investigations
• FBC, ESR, CRP• ANA (high sensitivity), anti-dsDNA (high specificity) • 25% RF +VE• Low complement (C3, C4)• Screen for renal disease• Antiphospholipid antibodies if APTT prolonged• CT/MRI - renal/neuro involvement
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SLE - management
• Patient education - avoiding sunlight, smoking cessation, planning pregnancies etc• CV risk reduction• NSAIDs for symptomatic relief• Steroids and antimalarials• Major organ involvement - immunosuppressive agents (e.g. azathioprine, methotrexate - NOT sulfasalazine (linked to drug-induced))• Rituximab in severe disease (not licensed) • Plasma exchange - aggressive/life threatening SLE
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CREST Syndrome
Calcinosis
Limited cutaneous form of systemic sclerosis
Raynaud’s Phenomeno
n
Oesophageal
Dysmotility
Sclerodactyly Telangiectasi
a
Associated with - +ANA, +ACA, PBCImmunosuppressivesSymptomatic relief
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Antiphospholipid Syndrome (APS)
• CLOTClot - arterial/venous thrombosis e.g. stroke, TIA, PE, DVTLivedo reticularis - cutaneous cyanotic vascularityObstetric loss Thrombocytopenia + prolonged APTT
• May be primary or secondary (most commonly to SLE)• Female > Male
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Sjögren’s SyndromeChronic autoimmune disease - lymphocytic infiltration of the exocrine glands -• Dry eyes (xeropthalmia)• Dry mouth (xerostomia)• Parotid swelling
Primary or associated with other conditions (RA, SLE, scleroderma)
Ix - include autoantibodies (Anti-Ro, Anti-La, ANA etc) and Schirmer test
Mx - Symptomatic (artificial tears, pliocarpine (artificial saliva)), role for hydroxychloroquine
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Polymyositis and Dermatomyosits
• Inflammatory myopathies of unknown aetiology• PM 40-60 years old, DM childhood• Inflammation of muscles (and skin in DM) and vessels that supply them• Subacute onset of proximal arm and leg weakness (rash in DM, face and trunk)• Ix - markers of muscle damage - CK, EMG, biopsy• Steroids - if non-responsive methotrexate, azathioprine, IV Ig (esp DM)
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Fibromyalgia
Unknown aetiologyFemale > MaleChronic widespread painFatigueSleep disturbanceProblems with concentration/memoryAssociated - depression, anxiety, functional bowel disorderRisks - stressManagement - CBT, analgesics (pregabalin), antidepressants
39
SteroidsAll steroid effects are due to altered gene
transcription
Cell
Nucleus
Steroid
Diffuses into cell as lipid soluble
GCR
GCR = glucocorticoid receptor
GCR/S complex = transcriptionfactor
Diffuses into nucleus and binds to DNA
Once bound - Blocks transcription of pro-inflammatory markerse.g. PLA2
Promotestranscriptionof anti-inflammatories
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Steroids (cont)
PLA2
Arachidonic Acid
Prostaglandins
Thromboxanes
Leukotrienes
COX
Lipoxygenase
Inflammatory mediators
Clotting
Pro-inflammatory
Formation inhibited by steroids
NSAIDs
+ other mechanisms - promoted transcription of anti-inflammatory proteins
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MSK OSCE Tips...
• Ask about pain (all examinations)• Remember the basics - introduce yourself etc• Try to practice on real patients, especially hands• Think what could be combined e.g. c. spine and shoulder (ankle and knee??)• If in doubt, look, feel, move• Know features of inflammatory vs mechanical pain and basic management - may have to explain treatment/disease process• Don’t panic!
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What we haven’t covered...
• Osteoporosis• Vasculitis• Osteomalacia• Vertebral Disc Degeneration• Primary/Secondary Bone Tumours, Myeloma• Mechanical Back Pain• Infection - Septic Arthritis, Osteomyelitis
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[email protected]@sheffield.ac.uk