Rheumatology PDF

Rheumatology Clinical sciences 1 AHS3004W Dr M.A De Souza Course Convenor Rheumatology module  ▪ Definitions, Epidemiology, signs and symptoms and management of: ▪ - Osteoarthritis ▪ - Fibromyalgia ▪ - Gout Learning ▪ -...

Rheumatology Clinical sciences 1 AHS3004W Dr M.A De Souza Course Convenor Rheumatology module  ▪ Definitions, Epidemiology, signs and symptoms and management of: ▪ - Osteoarthritis ▪ - Fibromyalgia ▪ - Gout Learning ▪ - Rheumatoid Arthritis outcomes ▪ - Ankylosing spondylitis ▪ - Juvenile idiopathic arthritis ▪ - Rheumatologic conditions in HIV  ▪ Osteoarthritis is a non-inflammatory, degenerative condition of joints. ▪ Characterized by degeneration of articular cartilage and formation of new bone i.e. osteophytes ▪ Characterized by metabolic, biochemical and structural changes in the articular cartilage Osteoarthritis and surrounding tissues that leads to structural failure and ulceration of the load bearing articular surface ▪ Slowly progressive disease in most patients ▪ It is common in weight-bearing joints such as the hip and knee ▪ Also seen in the spine and hands  Results from a complex interplay of multiple factors * joint integrity * genetic predisposition Osteoarthritis * local inflammation * mechanical forces * cellular and biochemical processes  ▪ Both males and females are affected ▪ More common in older females > 50 years particularly in post menopausal women Prevalence ▪ Most common joint disease in the world ▪ Affects the majority of people over the age of 65 ▪ Symptoms appear in middle age  ▪ Obesity ▪ Abnormal mechanical loading e.g. meniscectomy ▪ Inherited type II collagen defects in premature polyarticular OA ▪ Inheritance in Nodal OA ▪ Occupation e.g. Farmers Risk Factors ▪ Infection ▪ Poor posture ▪ Aging process in joint cartilage ▪ Defective lubricating mechanisms ▪ Incompletely treated congenital dislocation of the hips  ▪ Primary ▪ - more common ▪ - cause unknown, without any time of injury or cause ▪ - common in elderly ▪ - wear and tear Classification ▪ - localized or generalized ▪ Secondary ▪ - due to predisposing causes e.g. injury, previous infections, RA, obesity, deformity, hyperthyroidism  ▪ Nodal Generalized OA ▪ Crystal associated OA ▪ - mainly in elderly, women, often the knee ▪ - calcium pyrophosphate crystal deposition- CPPD Types of OA ▪ - makes it worse, more painful and more stiff ▪ OA of premature onset ▪ - Previous meniscectomy, haemochromatosis  ▪ OA is a degenerative condition primarily affecting the articular cartilage. Pathology ▪ There are affects on the bone, synovial membrane, capsule, ligaments and muscles  ▪ Localized joint pain- worsens with activity and relieved by rest ▪ ( severe disease may have pain at rest) ▪ Weight bearing joints may lock or give Symptoms way – advanced disease ▪ Stiffness in the morning or following inactivity rarely exceeds 30 minutes ▪ Pain worse at the end of the day  ▪ Bony enlargement ▪ Crepitus ▪ Cool effusions ▪ Decreased range of motion ▪ Tenderness on palpation at the joint line Signs ▪ Pain on passive motion ▪ Absent in OA is the boggy synovitis in inflammatory arthritis ▪ Distribution- more weight bearing joints but can involve the hands  ▪ Pain ▪ Stiffness ▪ Muscle spasm ▪ Restricted movement ▪ Deformity Clinical features ▪ Muscle weakness or wasting ▪ Joint enlargement and instability ▪ Crepitus ▪ Joint effusion  ▪ Usually slow onset of discomfort, with gradual and intermittent increase ▪ Pain is more on weight bearing due to stress on the synovial membrane and later on due to the bone surface which Pain and are rich in nerve endings tenderness ▪ Initially relieved by rest but later on disturbed sleep ▪ Diffuse/sharp and stabbing local pain  ▪ Possible causes ▪ * raised intra-osseous pressure ▪ * inflammatory synovitis ▪ * periosteal elevation Pain in OA ▪ * muscular changes ▪ * fibromyalgia/pain amplification ▪ * central neurogenic changes  ▪ Coarse crepitus: palpate/hear ( due to flaked cartilage and eburnated bone ends( bony sclerosis at areas of cartilage loss) ▪ Reduced ROM: capsular thickening and Other bony changes in joint ▪ Muscle spasm or soft tissue contracture ▪ Deformities- soft tissue swellings, osteophytes, joint laxity, asymmetrical joint destruction leading to angulation  ▪ History ▪ Examination ▪ Laboratory tests ▪ -* ESR –erythrocyte sedimentation rate Diagnosis ▪ -* Rheumatoid factor titers ▪ -* Evaluation of synovial fluid ▪ -* Radiographic study of affected joints ▪ ( X-rays versus MRI)  ▪ Osteophyte formation-most specific /advanced disease ▪ Joint space narrowing ▪ Subchondral sclerosis ▪ Cysts Radiological ▪ Bouchards nodes= are hard bony features of OA outgrowths or gelationous cysts on the proximal interphalangeal joints, often in men ▪ Heberden’s nodes= on the distal interphalangeal joint, more in women  ▪ Education ▪ Relieve symptoms, control pain and swelling Management ▪ Minimize handicap ▪ Limit progression, prevent disabilities  ▪ Education: obesity!!! ▪ Physiotherapy : exercise programs and pain relief modalities ▪ - exercise important for cartilage nutrition ▪ - some evidence lack of exercise leads Treatment to progression of OA principles ▪ - encourage full range low impact movements ▪ Aids and appliances ▪ Medical treatment ▪ Surgical treatment  ▪ Simple analgesics, low dose paracetamol and low dose ibuprofen ▪ NSAID’s prn/regular* ▪ Intra-articular corticosteroids Medical ▪ Tropical treatments e.g NSAID creams management ▪ Chondroprotective agents ▪ *Beware of the high risk of GI disease and peptic ulcers, renal insufficiency  ▪ Arthroscopic washout ▪ Joint debridement ▪ Bony decompression Surgical ▪ Osteotomy management ▪ Arthroplasty ▪ Joint replacement  ▪ Indications: pain affecting work, sleep, walking and leisure activities ▪ Complications: Joint ▪ - sepsis replacement ▪ - loosening ▪ - lifespan of materials ( mechanical failure) Questions  ▪ Chronic ▪ Systemic Rheumatoid ▪ Auto-immune disorder Arthritis ▪ Causing a symmetrical polyarthritis  ▪ A chronic inflammatory disorder that may affect many tissues and organs. ▪ It mainly attacks the joints producing an inflammatory synovitis ▪ May have inflammation in the lungs, pericardium, pleura and sclera Rheumatoid ▪ Cause is unknown but autoimmunity arthritis plays a big part in its chronicity and progression ▪ A chronic disease who’s pain intensity and deterioration of joint structures progress over time often leading to deformations and disability.  ▪ Affects -.5 to 1% of the population world wide ▪ Women 3x more than men ( pre menopause) ▪ More common in smokers ▪ Family history plays a role Epidemiology ▪ Genetic factors* ▪ Most commonly diagnosed between the ages of 40 and 50 years and no later than 80 years of age. ▪ Peak prevalence 30 to 50 years  ▪ Synovitis with thickening of the synovial lining ▪ Infiltration by inflammatory cells ▪ Generation of new synovial blood vessels is induced by angiogenic cytokines ▪ Activated endothelial cells produce adhesion molecules ▪ These expediate extravasation of Pathology leucocytes into the synovium ▪ Synovium proliferates and grows out over the cartilage ▪ Produces a tumor like mass called a pannus ▪ Pannus destroyds the the cartilage and subchondral bone producing bony erosions  ▪ Onset of pain ▪ Early morning stiffness (>30 min) ▪ Swelling in the small joints of the hands and feet ▪ As disease progresses there is Clinical features weakening of joint capsules ▪ - joint instablitity ▪ - subluxation ▪ - deformity  ▪ Arthritis of the joints – synovitis ▪ Joints become swollen, tender and warm and stiffness limits their movement ▪ Multiple joints ▪ Often small joints of hands , feet and Signs and cervical spine and larger joints such as shoulder and knees symptoms ▪ Synovitis can lead to tethering of tissue with loss of movement and erosion of the joint surface causing deformity and loss of function. ▪ Often symmetrical but initially can be asymmetrical  ▪ Trigger fingers ▪ Boutonniere deformity – middle PIP becomes stuck in a bent position and the MCP and DIP hyperextend ▪ Swan neck deformity – MCP and DIP Hand deformities abnormally flex and PIP hyperextends ▪ Hitchhikers thumb- MCP abnormally flexes while IP hyperextends ▪ Ulnar deviation- MCP dislocate towards ulnar side  ▪ Often subcutaneous, it is the feature Rheumatoid most characteristic of RA nodule  ▪ Systemic – fever , weight loss and fatigue ▪ Eyes- scleritis, perforation of the eye ▪ Neurological – carpal tunnel syndrome, alanto subluxation and cord Non- articular compression manifestations of ▪ Haematological – lymphadenopathy RA ▪ - Felty’s syndrome ( RA, spelenomegaly, neutropenia) ▪ - anaemia ▪ Pulmonary- pleural effusions, lung fibrosis, Rheumatoid nodules  ▪ Heart and peripheral vessels , pericarditis, pericardial effusions, Raynauds syndrome Non Articular ▪ Vasculitis – leg ulcers, gangrene of cont fingers and toes ▪ Kidneys –amyloidosis and nephrotic syndrome and renal failure  ▪ Blood tests- ESR raised and CRP raised ▪ - may have anaemia ▪ Rheumatoid factor (RF) ▪ - RF is a specific antibody in the blood ▪ *** a negative RF does not rule out RA. Its then called seronegative and often in Blood tests first year. ▪ Other tests like anti-citrullinated protein antibodies (ACPA’s) ▪ - only positive in a proportion ▪ - if positive then RA ( 95% specificity)  ▪ Joint narrowing ▪ Erosions at the joint margins X- rays  ▪ High neutrophil count in uncomplicated Synovial fluid disease  ▪ At least 4 criteria must be met: ▪ - morning stiffness >1 hour most mornings > 6 weeks ▪ - arthritis and soft tissue swelling >3 of 14 joints > 6 weeks ▪ - arthritis of the hand joints > 6 weeks ▪ - symmetric arthritis > 6 weeks Diagnosis ▪ - subcutaneous nodules in specific places ▪ - Rheumatoid factor at a level above the 95% percentile ▪ - Radiological changes suggestive of joint erosion (erosions , periarticular osteopenia)  ▪ Ruptured tendons ▪ Ruptured joints (Bakers cysts) ▪ Joint infections Complications ▪ Spinal cord compressions ▪ Side effects of therapy  ▪ No treatment cures RA ▪ Goals ▪ -remission ▪ -return of full function Management ▪ -maintenance of remission with disease modifying agents ▪ Effective management requires a multidisciplinary approach  ▪ Goal: alleviate the current symptoms and to prevent future destruction of the joints resulting in handicap ▪ DRUG therapy ▪ - cortisone ▪ - anti-inflammatory agents ▪ - drugs affecting the immune system Management ▪ OTHER ▪ - weight loss ▪ - OT ▪ - podiatry ▪ - physiotherapy ▪ - acupuncture  ▪ ACR diagnostic criteria ▪ - age < 16 years ▪ - arthritis of 1 or more joints Juvenile ▪ - symptoms of at least 6 weeks Rheumatoid ▪ - an onset type after 6 month of arthritis observation Juvenile Idiopathic ▪ * pauciarticular arthritis (JIA) ▪ * polyarticular ▪ * systemic ▪ - Exclusion of other forms of arthritis  ▪ Rare before age of 6 months Epidemiology of ▪ Peak age normally from 1 to 3 years JIA ▪ New cases throughout childhood  ▪ Begins with synovial inflammation ▪ Morning stiffness but may present as increased irritability, quarding of affected joints or refusal to walk Signs and ▪ Fatique, low grade fever, anorexia, symptoms weight loss and failure to grow ▪ Serositis, red eyes ▪  ▪ History and examination ▪ Blood tests e.g Rheumatoid factor Diagnosis ▪ X-rays and MRI  ▪ Drug therapy : ▪ - NSAIDs ▪ - Immune modulatory and biologics ( watch out for infections, side effects and avoid live vaccines) ▪ Supportive care, OT, physio, schools, opthalmology Management ▪ Goals: ▪ Achieve remission, minimize medication toxicity, maximize function, optimize growth and development and improve quality of life.  ▪ Form of arthritis that is long lasting ( chronic) and most often affects the spine ▪ It affects joints in the spine and the sacroilium in the pelvis causing Ankylosing eventual fusion of the spine spondylitis (AS) ▪ Complete fusion results in complete rigidity of the spine = bamboo spine ▪ Is a systemic rheumatic disease and is one of the negative spondyloarthopathies  ▪ Typically young men aged 18-30 ▪ Men to women 3:1 Epidemiology of ▪ Cause is unknown but genetic factors AS play a big role ▪ ( blood test HLA B27 gene)  ▪ Characteristic spinal changes and X- rays sacroiliitis  ▪ No cure ▪ General treatment ▪ - drug therapy including ▪ * anti-inflammatory drugs ▪ * DMARD ( disease modifying anti- rheumatic drugs) ▪ - used to reduce the immune system Management response through immunosuppression ▪ * TNF alpha blockers (antagonists) (biologics) ▪ - used in AS and other autoimmune diseases ▪ - most promising treatment  ▪ Surgery e.g osteotomy, arthroplasty Management  ▪ HIV- associated arthritis ▪ - nonerosive oligoarthritis ▪ - legs Rheumatologic ▪ - unknown cause conditions in HIV ▪ - 1% of patients ▪ - self limiting ▪ - less than 6 weeks  ▪ Reiter’s syndrome ( reactive arthritis) ▪ - more common in HIVpositive patients who are HLA-B27 positive Rheumatologic ▪ - treated with HIV suppression and TNF- conditions in HIV alpha antagonists  ▪ Septic arthritis Rheumatologic ▪ - mainly sternoclavicular and leg joints conditions in HIV  ▪ Gout Rheumatologic ▪ - hyperuricemia is common with HIV conditions in HIV ▪ - often from drugs  ▪ Rhabdomyolysis Rheumatologic ▪ - in primary HIV infection conditions in HIV ▪ - or complicate statin use in HAART  ▪ HIV- associated polymyositis ▪ - 2-7% of HIV patients with HIV ▪ Other Rheumatologic ▪ - Vasculitis conditions in HIV ▪ - SLE ▪ - Sarcoidosis ▪ - drug related