Condition 1 Flashcards
definition for osteoarthritis
clinical syndrome of joint pain involving degradation of bone. also known as degenerative arthritis
Who is affected the most by osteoarthritis
F 3x>M
>50s
causes for osteoarthritis
primary - unknown
secondary
- rheumatoid arthritis
- gout
- seronegative spondyloarthritis
- septic arthritis
- Paget’s disease of bone,
- avascular necrosis eg corticosteroid therapy,
- metabolic disease - chondrocalcinosis, hereditary haemochromatosis, arcomegaly
- systemic diseaes - haemarthrosis (due to haemophilia), haemoglobinopathies, neuropathies
pathogenesis of osteoarthritis
focal destruction of articular cartilage
cartilage destruction without any subchondral (layer of bone just below cartilage) bone response (atrophic disease) response or with massive new bone formation at joint margins (hypertrophic disease)
cartilage is constant regeneration and degeneration and balance is disrupter in OA so cartilage becomes oedematous - focal erosion develops
repair is attempted but disordered - surface become fibrillated and fissured
cartilage ulceration exposes underlying bone to increase production micro-fractures and cysts, bone attempts repair but produces abnormal sclerotic subchondral bone and overgrowths at the joint margins call osteophytes. also some secondary inflammation
macrophages releases VEGF leading neovasculation of the joint and this may bring new innervation of articular cartilage so pain even after inflammation has subsided
RF for osteoarthritis
Genetic - FH increased age Female Obesity - increase weight on joint joint injury/trauma/fractures occupational/recreational stresses on joints reduced muscle strength joint laxity joint mal-alignment osteoporosis
symptoms of osteoarthritis
joint pain
relieved by rest
worse on exercise
joint stiffness in the morning (lasting no longer than 30 minutes)
joint instability
localised disease - usually either knee or hip
generalisd disease - usually knees, DIPS, CPC of thumb
worsen during the day
signs of OA during exam
joint tenderness polyarticular (affecting more than 1 joint) crepitus limitation/decreased range of movement joint instability Heberden's node at DIp Bouchard's nodes at PIP mild synovitis
differentials for OA
rheumatoid arthritis - morning stiffness, pain worse on rest and better on exercise, symmetrical joint pattern
gout - acute, affects toes usually, mono/oligoarticular
ankylosing spondylitis - affect mainly spine, inflammatory back pain
septic arthritis - monarticular, red, hot, swollen
bursitis - monoarticular, morning stiffness, warm, red
investigation for OA
diagnosis usually clinical
bloods will be -ve for rheumatoid factor and anti-nuclear AB and otherwise normal but CRP maybe elevated
joint aspiration maybe considered to rule out other causes if swollen joint/effusion
advance disease can be seen on X-ray using the following nemonic
L - Loss of joint space
O - Osteophytes
S - Subarticular sclerosis
S - Subchondral Cysts
treatment for OA
treat symptoms and disability not the XR appearance
- education about condition - dec pain and inc compliance
- exercise, hydrotherapy, local heat, ice packs, NSAID gel
- Analgesia
- dec weight, walking aids, supportive footwear, physio
- intra-articular steroid injections help with symptom relief only if severe and only short-term improvement
- arthoscopic surgery is not beneficial, joint replacemnt is the ultimate best way –> surgery (replacemetn arthoplasty)
Definition of Rheumatoid arthritis
Autoimmune disease causing symmetrical polyarthritis with systemic involvement due to synovial inflammation
how common is RA
world-wide distribution affection 0.5-1% of population
inc prevalence in Indian population and dec in Chinese and black africans
inc prevalence in smoker
Who is affect the most by RA
F 2x> M
commonest onset = 50-60yrs
causes of RA
Genetics - 60% of disease, strong association to HLA-DR4 and HLA-DRB1, familial pattern with high concordance in monozygotic twins
gender - women before menopause 3x> men after menopause M=F - sex hormones
immunology - immune dysregulation plays a fundermental role in pathogenesis
Triggering antigen remains unclear
Pathogenesis of RA
widespread persisting synovitis (inflammation of synovial lining of joints, tendon sheaths or bursae)
Rheumatoid factor (RF) (autoAB with Fc portion of IgG as antigen) self-aggregate and form immune complexes and result in synovitis
production of rheumatoid factors in synovium by plasma cells are key.
synovium is usually thin but thicken in RA and become a palpable swelling around joints and tendons
synovium is infiltrated by a variety of inflammatory cells
vascular proliferation and inc permeability of blood vessels and synovial lining layer –> effusions
synovium become hyperplastic and spread from joint margins into cartilage surface which damages the underlying cartilage by blocking normal route for nutrition and direct effects of inflamm cells on chondrocytes
cartilage becomes thinning and underlying bone exposed - juxta-articular bony erosion on XR
Erosions then lead to deformities
symptoms of RA
joint pain worse on rest better with exercise morning stiffness symmetrical pattern affects mainly hands and feet then progresses to larger joints fatigue and weakness
less common presentation
Palindromic (periodic attack of RA and in between episode, symptoms disappear), 24-48hrs
transient - self-limiting disease - lasting less than 12 months and leaving no permanent joint damage
remitting - a period of several year during which arthritis is active but then remit, leaving minimal damage
chronic, persistent - most typical form, relapsing and remitting course over many years, tend to develop greater joint damage and long-term diability
rapidly progressive - rapidly progress over a few years and leads to rapidly developing severe joint damage and disability
signs of RA on exam
early - inflammation but no joint damage, joint swelling, look for tenosynovitis or bursitis
later - joint damage and deformity, ulnar deviation or the fingers and dorsal wrist subluxation, Boutonniere or swan neck deformity of fingers, Z deformity of the thumb, hand extensor tendons may rupture foot changes are similar
extra-artiuclar - nodule on elbows, forearms or lungs, vasculitis, fibrosing alveolitis, pleural and pericardial effusions, raynaud’s, carpeal tunnel syndrome, peripheral neuropathy, splenomegaly, scleritis, osteoporosis, amyloidosis
differential for RA
osteoarthritis - worse on exercise, better on rest, morning stiffness <30minutes, heberdon’s/bouchard’s nodes
gout - acute, mono/oligo-articular, extremely painful
septic arthritis - red, hot, swollen joint, monoarticular
viral arthritis
reactive arthritis
polymyalgia rheumatic
any other systemic disease presenting with arthropathy eg SLE, infective endocarditis
investigation for RA
diagnostic tool available (see core-condition 2), 6/10 is diagnostic
blood - anaemia, inc ESR and CRP are useful in monitoring treatment
serology - RF +ve in 70% (presence.absence of RF does not rule in/out disease but good predictor
XR of affected joint - establish a baseline (only soft tissue swelling is seen in early disease)
aspiration of joint - if an effuson, would look cloudly due to presence of white cells
treatment for RA
No cure but many drugs available to prevent deterioration
symptom control =
- NSAIS and coxibs
- night sedation maybe needed
- corticosteroids (slows the course of disease)
- intra-articular injection with semi-crystalline steroid (sort lived), intramuscular depot injection (methylprednisolone) - helps to control severe flare ups and possibly prophylactic
DMARDS (Disease-modifying antirheumatic drugs) =
- mainly act through cytokine inhibiton to dec inflammation, swelling and development of joint erosions and irreversible damage; but slow-acting agents
- sulfasalazine, methotrexate, hydroxychloroquine (best result achieved through combination
- leflunomide
- biological DMARDs - TNF alpha blocker - Ethanercept, adalimumab, infliximab (mAB)
- drugs not commonly used - IM gold, azathioprine, cyclosporine, penicillamine
encourage regular exercise (in a hydrotherapy pool) etc
surgery can be considered in severe cases to remove pain
definition of gout
an inflammatory arthritis due to deposition of monosodium urate (MSU) monohydrate crystals within joints causing acute inflammation and eventual tissue damage. It has been described as one of the most painful acute conditions a human being can experience
how common is gout
not that common, 60% big toe
