wk 7- joint pain Flashcards
what make up the synovial joint
bone
cartilage covering articular surfaces
synovial fluid
synovial joint capsule
what is OA
a chronic, degenerative synovial joint condition which is characterised by loss of articular cartilage and periarticular bone response
more common in women
patho of OA
has both mechanical and biological factors to it
mechanical: abnormal loading/wear such as injury, instability, hypermobility, joint dysplasia play a role, deformity, sport, obesity
biological: genetic predisposition, age related changes to cartilage metabolism
- transmission of inflammatory mediators from synovial fluid into cartilage causing an inflammatory reaction/damage
- progressive chondrocyte death and cartilage destruction occur
- subchondral bone undergoes infarction forming bone cysts
- attempts of repair to stabilse the joint cause subchondral sclerosis and marginal osteophytes
- inflammation of synovium and periarticular soft tissues
what can reduce OA of knee
weight loss
by 33% if they drop down a weight class for women
by 25.4% for men
features of OA
pain by activity and relieved by rest
rest stiffness developed over time
joint tenderness
swelling
crepitus
restriction ROM
radiographic features
- non uniform joint space narrowing
-osteophytes
-subchondral sclerosis
-subchondral cysts
-loose bodies
-sublaxation
OA management
- exercise -maintains ROM and strengthens muscles
- footwear/ assistive devices- cranes, brace, splints, footwear
- weight loss (esp knee)
pharma
1. NSAIDs non selecitve or cox2 with or without SSRI/SNRI
2. opiods for short term use
3. corticosteroid/hyaluronic acid injections for short term use
- surgery: joint replacement
what is synovial chondromatosis
synovium grows abnormally and produces nodules made of cartilage . nodules can sometimes break off and become loose bodies inside the joint which can damage the smooth articular cartilage
rare condition that can lead to OA
what is RA
systemic, inflammatory, autoimmune disease
more common in females, with a reduction in life expectency
RA patho
Triggered by a genetic and environment factor
- synovial plasma cells produce antibodies that form immune complexes and stimulate leucocyte proliferation
- T cells infiltrate the synovium and secrete cytokines which recruits more inflammatory cells like macrophages into the joint which secrete more cytokines
- This stimulates pannus formation of the synovial membrane which causes destruction of cartilage, bone and soft tissue
what causes RA to occur
cause is unknown but there are
- genetic (50% of risk)
- environmental risk factors
- smoking
-infections
-diet
-air pollution
-silica exposure
-alcohol
-obesity
clinical features of RA
symmetrical
presents insidiously
multiple joints
joint swelling
warmth
stiffness after inacitvity
pain
prolonged morning stiffness )>60mins)
complications of foot for RA
Common deformities: pes planus, plantar fasciopathy, tib post/achilles tendonitis , hallux valgus, hammer toes
rheumatoid nodules at sites of pressure in 30% of patients
complications of RA extra articular
- vascular complications
-neuropathy in half the cases
-nodules
-ulcers
-infection
-eye complications
-anaemia/iron deficiency
-muscle disorders
how do you detect an active disease in RA
- lateral squeeze test
- swollen joint count
- exam and palpation of tendons and bursae
early referral for RA criteria
- 3+ swollen joints
- squeeze test positive for MTP and or MCP
- morning stiffness 30mins or more
RA management
- referral to rheumatologist - early diagnosis improves outcomes
pharma: conventional synthetic disease modifying anti rheumatic drugs
- methotrexate oral or subcutaneous injection once weekly
2.Leflunomide, sulfasalzine and hydroxychloroquine may be used alone or in combination - corticosteroids are used to manage symptoms until antirheumatic drugs begin
- biological disease modifying anti rheumatic drugs (infliximab)
- increased risk of infections
- biological disease modifying anti rheumatic drugs (infliximab)
- immunisations
gout what is it
inflammatory arthritis associated with hyperuricaemia and uric acid crystals
common in men at the 1MTPJ
risk factors for gout
- alcohol
-diet of purines (red meat, seafood)
-aspirin, diuretics, cytotoxic drugs (that raise plasma urate levels)
-fam history
-conditions
gout patho
hyperuricaemia occurs through
1. decreased renal urate excretion- alcohol
2. increased urate production
3. or increased intake - purine rich foods
monosodium urate crystals may occur in response to an event
diagnosis of gout
- serum urate (not reliable because levels may be dropping after attack)
-US imaging
features of gout
- 1st mTPJ
-Swollen, hot, red joint
-tender
-tophi (chronic)
-unable to weightbare
-loss of ROM
management for gout
- rule out septic arthritis
- NSAIDs/prednisone/local corticosteroid injection
- urate lowering medication if 2+ attacks within a year
- bloods checked every 4-6 weeks after attack
