joints 1 Flashcards
osteoarthritis
aka degenerative joint disease
characterized by degeneration of cartilage, failure of repair -> failure of synovial joints
osteoarthritis morphology
water content increases, proteoglycans decrease
granular soft articular surface
pieces break off- joint mice
bone eburnation
osteoarthritis clinical
usually doesn’t become symptomatic until >50
deep, achy pain, worsens with use, morning stiffness, crepitus, limited ROM
impingement of spinal foramina -> nn compression
usually only a few joints involved
heberden nodes
prominent osteophytes at distal interphalangeal joints common in women, not men
RA
chronic inflammatory disorder of autoimmune origin
principally attacks joints producing nonsuppurative proliferative and inflammatory synovitis
common hand presentation of RA
ulnar deviation and large knuckles
CD4 cells and RA
T helper cells may initiated autoimmune response in RA by reacting with an arthritogenic agent (microbial or selfAg?)
TNF and RA
most firmly implicated mediator of the disease
TNF antagonists very effective Tx
Germinal centers
found in synovium of RA pts with secondary follicles and abundant plasma cells producing Abs (some are against selfAgs)
pannus
mass of edematous synovium, inflammatory cells, granulation tissue, and fibroblasts that grow over articular cartilage and causes erosion -> fibrous ankylosis which eventually ossifies -> bony ankylosis
specific to RA
RA and skin
RA subQ nodules are most common cutaneous lesions
ulnar aspect of forearm, elbows, occiput, lumbosacral area,
can form in lungs, spleen, heart
Rheumatoid nodules
firm nontender, round-oval
microscopically resemble necrotizing granulomas with central zone of fibrinoid necrosis surrounded by macros, Ts, and Bs
RA and blood vessels
vasculitis
high rheumatoid factor correlates with risk of vasculitis
what should you check synovium sample for before Dx RA
acid fast stain for mycoplasm (both cause necrotizing granulomas)
RA clinical
50% have insidious onset with malaise, fever, fatigue, after several months joints involved
generally symmetrically and smaller joints first
Dx of RA
X-RAY
sterile, turbid, synovial fluid, decreased viscosity, poor mucin clot formation, inclusion bearing neutrophils
combination of Rheumatoid factor and anti-CCP Ab
juvenile idiopathic arthritis
presents <16 and persists for at least 6wks
JIA vs RA
In JIA:
-oligoarthritis is more common
-systemic disease more frequent
-large joints are affected more then small
-rheumatoid nodules and rheumatoid factor are usually absent
ANA Ab is usually +
spondyloarthropathies
ankylosing spondyltis psoriatic arthropathy juvenile anklosing spondylitis sacroilitis intestinal arthropahty, UC, Chrons reactive arthropathy, reiter syndrome
spondyloarthropathies general characterisitics
pathologic changes in ligamentous attachments rather then synovium
involvement of SI w/or w/o other joints
absence of rheumatoid factor
HLA-B27
Ankylosing spondyltis
destruction of articular cartilage and bony ankylosis especially at SI and apophyseal joints
symptomatic 2nd-3rd decade of life as lower back pain and spinal immobility
90% are HLA-B27+
reactive arthritis
arthritis, nongonococcal urethritis/cervicitis and conjunctiviits
ususally men 20-30
80% HLA-B27+
also seen in HIV
what organisms are linked to reactive arthritis
chlamydia shigella salmonella yersina campylobacter
enteritis associated arthritis
yersinia, salmonella, shigella, campylobacter
appears abruptly usually at knees and ankles, but sometimes also wrists, finger, toes
lasts for 1yr, generally clears rarely accompanied by ankylosing spondylitis
