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…

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

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

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

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

Osteoarthritis - x-ray

• Osteophyte• Joint space narrowing• Subchondral Sclerosis• Subchondral Cysts

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

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)

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

Crystal ArthropathyText

Rheumatoid Arthritis: Pathophysiology

Rheumatoid arthritis is a chronic, systemic,

inflammatory disease of unknown aetiology that

primarily affects the peripheral joints in a symmetrical pattern

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

Rheumatoid Arthritis: Hands

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

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)

Seronegative spondyloarthropathies

Ankylosing SpondylitisPsoriatic ArthritisReactive ArthritisEnteropathic Arthritis

HLA B27

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

Ankylosing Spondylitis

X-ray findings Fusion of vertebral bodies (‘Ankylosing’) - late stageJuxta-articular sclerosis, erosions, widening of sacroiliac jointsSyndesmophyte formation, ‘bamboo spine’

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

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

Psoriasis

Red, silver-scaled lesions - predominately extensor surfaces and scalp

Nails - pitting, yellowing, onycholysis, leukonychia, transverse ridging

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

Enteropathic Arthritis

Arthritis associated with IBD

Systemic Lupus Erythematous

SLE is a chronic, autoimmune, inflammatory,

multisystem, connective tissue disorder that can

affect almost any system in the body

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)

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

SLE - presentation

Malar Rash

Discoid Rash

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

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

CREST Syndrome

Calcinosis

Limited cutaneous form of systemic sclerosis

Raynaud’s Phenomeno

Oesophageal

Dysmotility

Sclerodactyly Telangiectasi

Associated with - +ANA, +ACA, PBCImmunosuppressivesSymptomatic relief

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

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

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)

Fibromyalgia

Unknown aetiologyFemale > MaleChronic widespread painFatigueSleep disturbanceProblems with concentration/memoryAssociated - depression, anxiety, functional bowel disorderRisks - stressManagement - CBT, analgesics (pregabalin), antidepressants

SteroidsAll steroid effects are due to altered gene

transcription

Nucleus

Steroid

Diffuses into cell as lipid soluble

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

Steroids (cont)

Arachidonic Acid

Prostaglandins

Thromboxanes

Leukotrienes

Lipoxygenase

Inflammatory mediators

Clotting

Pro-inflammatory

Formation inhibited by steroids

NSAIDs

+ other mechanisms - promoted transcription of anti-inflammatory proteins

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!

What we haven’t covered...

• Osteoporosis• Vasculitis• Osteomalacia• Vertebral Disc Degeneration• Primary/Secondary Bone Tumours, Myeloma• Mechanical Back Pain• Infection - Septic Arthritis, Osteomyelitis

mda10jrm@sheffield.ac.ukmda10elw@sheffield.ac.uk

phase 2 erin whyte jamie mcconnell rheumatology the peer teaching society is not liable for false or...

painthe peer teaching

pipthe peer teaching

joint line

line nsaids

joint injury

joint involvementtmj

aspiration nsaids

topical nsaids

Documents

caspers whyte i

4679385 blues [mcconnell]

mcconnell pastoral letter

mcconnell, oma, adversary

mcconnell cap3

william whyte

caspers whyte ii

mcconnell cap2

whyte smart apartment power

mcconnell family020505

whyte 10 4 1

misleading advertisements

misleading language

calendar | mcconnell & jones

whyte street corner society

fiona preston-whyte - escience associates participation...1...

jack whyte - ordinul templierilor

queensland major contractors association · decmil laing...

misleading invoices

mqug2015 july richard whyte