Joints Flashcards
(44 cards)
Osteoarthritis: primary and secondary causes
degenrative joint disease DJD
idopathic (primary) with aging
men: hips predominate
women: knee and hands predominate
secondary: repeated injuries to a joint, hemochroatosis, obesity
Osteoarthritis: etiology
Degeneration of cartilage outpaces repair. 80-90% by age 65. Mechanical defects due to muscle strength or obesity.
Osteoarthritis phases
chondrocyte injury
chondrocyte proliferate
chondrocyte drop out with a loss of cartilage
Osteoarthritis presentation on the bone
superficial roughened and cracked cartilage.
bone eburnation (exposed bone on surface0 looks like polished ivory and underlying bone sclerosis
joint mice (loose bodies of cartilage)
subchondral cysts of synovial fluid
ostephytes (bone spur): extra bone at joint edge
osteoarthritis presentation
insidious typically involving one or a few joints. Deep achy pain. morning stiffness. worse with use. creptius of joint. limited range of motion. vertebral osteophytes impinge on nerve root.
herberden nodes: osteophytes at DIP in women.
Osteoarthritis areas of risk
hips
knees
lower lumbar
cervical
dip
pip
first carpmetacarpal
spares: wrists, elbows, shoulders
Rheumatoid arthritis. etiology, gender, and age risk factor
systemic autoimmune inflammatory disease
nonsuppurative proliferative inflammatory synovitis often destroying cartilage with later ankylosis of the joint
female > male
age: any but most often 40-70
some genetic susceptibility
Rheumatoid arthritis: pannus
exuberant inflamed synovium
chronic inflammation with T cells 9mostly CD4), B cells, plasma cells, macrophages
granulation tissue with hemosiderin
erodes articular cartilage
erodes bone: juxtarticular cysts, subchondral cysts, osteoporosis
Rheumatoid arthritis pathogenesis
AG exposure in a susceptible host creating an ongoing autoimmune process. 80% have rheumatoid factor (autoAB against Fc portion or IgG) but is not specific. AB to citrullin modified peptides (anticyclic citrullinated peptide or CCP Ab) more specific
TNF major role
Synovial fluid: high protein content, low mucin content, inflammation
Rheumatoid arthritis: clinical presentation joints and spread
clinical course variable: can have periods of remission
10% acute onset but most insidious. May be preceded by malaise, fatigue, myalgia
symmetric with small joints before large. PIP MCP, MTP (note OA is DIP). Later writs, ankles, elbow, knees (spares hips)
joints: swollen, warm painful and stiff with inactivity
Rheumatoid arthritis diagnosis X ray and other features
X ray: juxta articular osteopenia. Bone erosions with narrowing of joint space from loss of articular cartilage. Joint effusions.
Radial deviation of wrist
ulnar deviation of fingers
flexion hyperextension of fingers (swan neck; boutonniere)
synovial cysts: Baker cyst (back of knee)
Rheumatoid arhtritis: clinical features: rheumatoid nodules
most common cutaneous manifestation (25%)
areas subject to pressure: ulnar aspect of forearm, elbow, occiput, lumbrosacral
fibrinoid necrosis surrounded by macrophages
Rheumatoid arthritis: clinical features: blood vessels
vasculitis: does not involve kidneys.
Can be obliterative endarteritis of vasa nervorum and digital arteries (neuropathies, ulcers, and gangrene).
Leukocytoclastic venulitis (purapura, skin ulcers, and nail bed infarction)
may be adjacent tendonitis, myositis
Rheumatoid arthritis critera
four of the following
AM stiffness
> 2 joints arthritis
typically and joint involvement
symmetric arthritis
rheumatoid nodules
serum rheumatoid factor
typically radiologic changes
Juvenile idiopathic arthritis: overview. Joint targets and other manifestations
Heterogeneous group by definition before age 16 and presents 6 weeks of oligoarticular < 5 joints, polyarticular, systemic
knees, writs, elbows, ankles (large joints)
extra articular manifestations: pericarditis, myocarditis, pulmonary fibrosis, uveitis, glomerulonephritis, growth retardation
Juvenile idiopathic arthritis vs Rheumatoid arhtritis
differs: oligoarthritis is more common. systemic onset more common. large joints. absence of rheumatoid factor, absence of rheumatoid nodules, may be ANA positive.
similiar: Pannus formation. Morphology of involved joints.
seronegative spondyloarthropathies
pathology in ligamentous attachment
immune mediated; no specific autoantibody. Many are +HLA B27. Rheumatoid factor negative.
seronegative spondyloarthropathies triggers and the types (4)
often triggered for example infection
- ankylosing spondyloarthritis
- enteritis associated arthritis
- reactive arhtritis
- psoriatic arthritis
Ankylosing spondyloarhtritis: risk factors gender, age, genetics, and affected area.
“rheumatoid spondylitis”
young adults; M>F
HLA B27 (90%)
axial joints: sacroiliac joint and apophyseal joints of vertebrae
Ankylosing spondyloarhtritis: onset, clinical presentation, complications
ONset 2-3 decade with low back pain
inflammation of tendon/ligament insertion: ossification of inflammation. Fibrous and boney ankylosis
complication: 1/3 hip, knee, shoulder arthritis. Uveitis, aortitis, amyloidosis, spine fractures
reactive arthritis (reiter syndrome) caused by and triad
appendicular noninfectious arthritis
< 1 month after primary infection. Genitourinary chlamydia or GI: shigella, salmonella (diarrhea)
triad: arthritis, urethritis or cervicitis (nongonococcal), and conjunctivitis
Reiter syndrome risk factors age and genetics. Areas of damage and clinical features.
20-30s
HLA b27 (80%)
ankles, knees feet (lower extremity) in asymmetric pattern
sausage toe or finger from digital tendon sheath synovitis
Reiter syndrome: other clinical features and SX patterns
extra articular: balantitis, conjunctivitis, heart conduction defects, aortic regurgitation
SX wax and wane with 50% recurrence
Enteritis assoiciated arthritis
GI infection by yersinia, salmonella, shigella, campylobacter. Liposaccharide stimulate immune repsonse.
most often abrupt in knees and ankles
generally clears in < 1 year