Rheumatology Flashcards
What is OA?
Osteoarthritis (OA) is a degenerative joint disease that is characterized by the breakdown of cartilage in the joints, leading to pain, stiffness, and reduced mobility.
What is the cause of OA?
The exact cause of OA is unknown, but risk factors include age, obesity, joint injury, and genetics.
Features of OA?
Pain - gradual onset, pain worsened by weight baring activity, deep, aching or throbbing pain
Joint stiffness - Gelling phenomenon: Prolonged inactivity may lead to temporary joint stiffness
Joint swelling
Crepitus
Joint instability
Varus/valgus deformities: Malalignment due to asymmetric joint space narrowing and osteophyte formation can occur in the knees.
Herberden’s nodes - Bony enlargements at the distal interphalangeal joints seen in hand osteoarthritis.
Bouchard’s nodes - ony enlargements at the proximal interphalangeal joints seen in hand osteoarthritis.
Limited ROM
XR features of OA?
decrease of joint space
subchondral sclerosis
subchondral cysts
osteophytes forming at joint margins
Diagnosis of OA clinically?
patient is > 45 years
has exercise-related pain
no morning stiffness or morning stiffness lasting < 30 minutes
Most common joints effected in OA?
Large weight-bearing joints (hip, knee)
Carpometacarpal joint
DIP, PIP joints
Typical history of OA vs RA?
OA
Pain following use, improves with rest
Unilateral symptoms
No systemic upset
RA
Morning stiffness, improves with use
Bilateral symptoms
Systemic upset
XR findings of RA?
Loss of joint space
Juxta-articular osteoporosis
Periarticular erosions
Subluxation
Common Joints in RA?
MCP, PIP joints
Management of OA?
Lifestyle - weight loss, muscle strengthening and general aerobic fitness
Topical NSAIDs
Oral NSAIDs with PPI
NICE recommend we do not offer paracetamol or weak opioids, unless: NICE
they are only used infrequently for short-term pain relief and
all other pharmacological treatments are contraindicated, not tolerated or ineffective
walking airs
Intraairticular steroids
Surgery
What is Rheumatoid arthritis?
Rheumatoid arthritis (RA) is a chronic, systemic autoimmune disorder characterized by symmetrical inflammation of the synovial joints, leading to progressive joint destruction, disability, and extra-articular manifestations.
Aetiology of RA?
Genetic factors
Environmental factors - smoking, infections (EBV, parvovirus)
Clinical features of RA?
Symmetrical joint involvement
Morning Stiffness
Joint swelling
Fatigue
Constitutional symptoms (fever, malaise, weight loss)
rheumatoid nodules, interstitial lung disease, keratoconjunctivitis sicca, and anemia of chronic disease.
Investigations for RA?
Rheumatoid factor (+ve in 70% of patients - high levels are associated with severe progressive disease)
Anti-CCP (may be detectable for up to 10 years before the development of RA) - higher specificity - 90-95%
what other conditions have a positive RF?
Sjogren’s syndrome (around 100%)
Felty’s syndrome (around 100%)
infective endocarditis (= 50%)
SLE (= 20-30%)
systemic sclerosis (= 30%)
general population (= 5%)
rarely: TB, HBV, EBV, leprosy
How is RA clinical diagnosed?
with the 2010 American college of Rheumatology criteria
how is Psoriatic arthritis different from RA?
PsA is another inflammatory arthritis that may mimic RA. However, it is typically associated with psoriasis and often affects skin and nails as well as joints.
Unlike the symmetrical polyarticular pattern commonly seen in RA, PsA often demonstrates an asymmetric oligoarticular pattern. Dactylitis (sausage digits) and enthesitis are also unique features of PsA that help differentiate from RA.
Radiographic findings such as pencil-in-cup deformity or periostitis could aid differentiation; these are not typical for RA.
How can you differentiate SLE from RA?
SLE is a chronic autoimmune disease that may present with arthralgia similar to RA but usually exhibits a wider range of systemic symptoms including malar rash, photosensitivity, oral ulcers, serositis, renal and neurological involvement.
SLE arthritis is typically non-erosive and does not lead to the joint deformities commonly observed in RA. Joint involvement in SLE is often migratory and transient.
Presence of autoantibodies such as antinuclear antibodies (ANA), anti-double stranded DNA (anti-dsDNA) or anti-Smith (anti-Sm) are more suggestive of SLE than RA.
Management of RA?
They now recommend DMARD monotherapy +/- a short-course of bridging prednisolone. In the past dual DMARD therapy was advocated as the initial step.
Monitoring response to treatment
NICE recommends using a combination of CRP and disease activity (using a composite score such as DAS28) to assess response to treatment
DMARDS - methotrexate, sulfasalazine, hydroxychloroquine
TNF inhibitors (indicated when there has been inadequate response to at least two DMARDs)
Rituximab
Complications of RA?
espiratory: pulmonary fibrosis, pleural effusion, pulmonary nodules, bronchiolitis obliterans, methotrexate pneumonitis, pleurisy
ocular: keratoconjunctivitis sicca (most common), episcleritis, scleritis, corneal ulceration, keratitis, steroid-induced cataracts, chloroquine retinopathy
osteoporosis
ischaemic heart disease: RA carries a similar risk to type 2 diabetes mellitus
increased risk of infections
depression
Less common
Felty’s syndrome (RA + splenomegaly + low white cell count)
amyloidosis
Hand deformities in RA?
Ulnar drift: Fingers lean away from the thumb and toward the pinky
Swan-neck deformity: The base and top joint of the finger bend downward, but the middle joint is straight
Boutonnière deformity: Also called a buttonhole deformity, the middle finger joint bends downward, while the top finger joint bends away from the palm
Hitchhiker’s thumb: The top part of the thumb arches far backward
