OA+ RA Flashcards
ACPA
Anti-cyclic citrullinated protein antibody- found in RA
Arg is modified by PAD to citrulline; antibodies formed against this.
Sx at the joint in RA
Pain, swelling, morning stiffness lasting > 1 hour that improves with use
Deformities
Rheumatoid nodules
2 mechanisms of bone loss in RA
1) Pannus- erodes bone + cartilage
2) Inflammatory cells simulate osteoclasts at synovial insertion sites- results in generalized bone loss
Displacement of capital femoral epiphysis from femoral neck
Slipped capital femoral epiphysis
Hyperextension of PIP w/ flexion of DIP
Swan-neck deformity; seen in RA
Heberden nodes/ Bouchard nodes and how do they present
Heberden nodes: osteophytes at the DIP joint
Bouchard node: osteophytes at the PIP joint
Presents as enlargement + thickening of DIP/PIP
Joint/ bone findings of OA (3)
1) Bone eburnation
2) Subchondral cysts/ sclerorsis
3) Joint space narrowing
Felty’s syndrome
RA + Splenomegaly + pancytopenia
HLA associated w/ RA
HLA-DR4
Extra-articular manifestations of RA
1) systemic sx (fever, fatigue, weight losss)
2) Cardiac- autoimmune process affects pericardium (MI, pericardial effusion)
3) Pulmonary- inflammation of pleura (pleurtiis, effusions, interstitial fibrosis)
4) Ocular- Sjogren’s, keratoconjunctivitis sicca (dry eye)
5) Felty’s syndrome
6) Anemia of chronic disease
7) Secondary amyloidosis
Why smoking/silica is associated with increased risk of RA
Inflammatory process in lungs causes production of peptidyl arginine deaminases (PAD), which forms citrullinated peptides; antibodies against these peptides involved in pathogenesis
Histology of OA
Disorganized + fragmented “joint mice” cartilage
3 consequences of loss of articular cartilage in OA
1) Development of subchondral bone cysts
2) Increased subchondral bone thickness (suchondral sclerosis) due to exposure of underlying bone
3) Formatino of osteophytes at the joint margins
Non-reducible flexion at PIP w/ hyperextension of DIP
Boutonniere deformity; seen in RA
Marker of tissue damage + disease activity in RA
Rheumatoid factor
Pannus
In RA, inflamed granulation tissue within synovium due to inflammatory process which leads to erosion of bone + cartilage
Findings of cervical subluxation and disease associated
Associated w/ RA
Inflammation of cervical joints can cause vertebral misalignment –> neurological dysfunction, problems w/ flexion of neck
IgM autoantibody against body’s own IgG
Rheumatoid factor
Pattern of joint involvement in RA
Symmetric joint involvement classically at small joints of hands + feet (most common- wrist, MCP, PIP); also occurs at elbows, ankles, and knees. DIP joints are spared!
Pattern of joint involvement in OA
Asymmetric usually affecting hips, lower lumbar spine, knees, and DIP/PIP
Most common areas of osteophyte formation in OA
DIP joints (Heberden nodes) + PIP joints (Bouchard joints) of fingers
Etiology of osteonecrosis
CAST Bent LEGS
Corticosteroids, alcoholism, sickle cell disease, Trauma (fracture), “The Bends” (Caisson/ decompression disease), Legg-Calve-Perthese disease, Guacher disease, slipped capital femoral epiphysis
Idiopathic avascular necrosis of femoral head
Legg-Calve-Perthes DIsease
Presentation of OA
1) Joint pain/stiffness in the morning that worsens w/ activity (gets worse during the day) and relieved by rest
2) Enlargement and thickening of joints- due to osteophyte formation (e.g Heberden + Bouchard nodes)
No systemic manifestations
Physical exam findings in RA
1) Fusiform swelling- soft tissue swelling (not due to bone growth); tender + warm, “boggy” feel
2) Deformities (Boutonnier, Swan-neck, ulnar finger deviation)
3) Rheumatoid nodules on extensor surfaces
4) Cervical subluxation
Most common site for osteonecrosis and why
Femoral head- due to insufficiency of medial circumflex artery
