seronegative arthritis Flashcards
ankylosing spondylitis
marie-strumpell disease
inflammatory arthropathy of the axial skeleton
can lead to fibrosis, calcification and ossification w/ fusion of the involved joints
primarily men b/w 15-30
ankylosing spondylitis etiology
about 90% of those with AS are HLA-B27 positive
human leukocytic antigen
ankylosing spondylitis pathogenesis
marked by a chronic non granulomatous inflammation
ankylosing spondylitis clinical manifestations
moving is important b/c they are in pain and then typically don’t want to move and can develop bamboo spine
lose of curvature of the cervical spine
ankylosing spondylitis diagnosis
MRI
short tau inversion, “Square sharpe vertebral column”
ankylosing spondylitis treatment
NSAIDs
DMARDs
TNF-ALPHA (effective in preventing progression by decreasing activity, inflammation and improve spinal mobility)
ankylosing spondylitis PT intervention
strengthen of trunk extensors = prevent flexion
exercise is very important
Reiter’s syndrome
reactive arthritis
arises after an infectious process at a site remote from the primary infection
usually follows venereal disease or an episode of bacillary dysentery and is associated w/ typical extraarticular manifestations
what are the most common microbial pathogens of reiter’s syndrome
shigella
salmonella
yersinia
campylobacter
chlamydia
who is affected the most by reiter’s syndrome
men in their 30s
classical triad of symptoms reiter’s disease
urethritis
conjunctivitis
arthritis
combination of peripheral arthritis w/ urthritis lasting long that 1 month is necessary before the diagnosis can be confirmed
treatment of reiter’s syndrome
NSAIDs
psoriatic arthritis
seronegative inflammatory joint disease affecting a small percentage of people who have psoriasis
associated w/ radiographic evidence of periarticular bone erosions and occasional significant joint destruction
when does psoriatic arthritis present
during the 2nd and 3rd decades of life
w/ onset of the arthritis occurring up to 20 years later
psoriatic arthritis pathogenesis
lymphocyte infiltration into the synovium
initially synovium is pale
with edematous granulation tissue extending along the continuous bone, eventually the synovium becomes thickened with villous hypertrophy, and may become filled with dense fibrous tissue in severe cases
psoriatic arthritis clinical manifestations
Commonly involves the DIP joints of the hands, although other joints of the digits may be involved including breaking of the nails
The joint changes may lead to significant hand deformities, including claw deformity
PT intervention for psoriatic arthritis
maintain mobility, pain control, decrease amount of joint damage
osteoarthritis
Degenerative joint disease is a slowly evolving articular disease that appears to originate in the cartilage and affects the underlying bone, soft tissues, and synovial fluid
primary and secondary
OA is the most common indication for total joint replacement
primary OA
is a disorder of unknown cause, and the cascade of joint degeneration events associated with it is thought to be related to a defect in the articular cartilage
secondary OA
has a known cause, which may be trauma, infection, hemarthrosis, osteonecrosis
OA etiology & risk factors
genetics
nutrition/weight
estrogen use
bone density
biomechanical factors
risk factors: smoking, genetics
secondary: sports that involve high intensity, acute, direct joint impact from contact w/ other players
OA pathogenesis
Tissue changes in OA are the result of active joint remodeling processes involving an imbalance between catabolic and anabolic repair activity
Presence of C-reactive protein and essential inflammatory cytokines, such as IL-1beta and TNF-alpha
OA clinical manifestations
Bony enlargement, limited range of motion, crepitus on motion
Characteristic Hand Deformities
Heberden’s Nodes: DIP
Bouchard’s Nodes: PIP
OA pharmacology
most common indication for a total joint replacement per pain/function
analgesics (acetaminophen) and topical capsaicin and glucosamine/chondroitin NSAIDs
DMOADs (disease modifying OA drugs)
viscosupplements (drugs that attempt to improve the viscosity and function of synovial fluid)
Glucosamine and Chondroitin Sulfate: agents that serve as precursors to the normal constituents of joint tissues, increased amounts of these ingredients should facilitate the repair of joint tissues
OA PT intervention
manual pt and supervised exercise
instruct body mechanics
ice per mild swelling
aquatic therapy
neurogenic arthropathy
charcot’s disease
chronic progressive degeneration of stress-bearing portion of a joint association w/ loss of proprioceptive sensation in the joint
damage to the nerves that supply the joint
avascular necrosis
osteonecrosis and aseptic necrosis are other names
the death of bone as a result of loss of blood supply in the absence of infection
femoral head is most common site
what does necrosis result from
tissue ischemia brought on by the impairment of blood conducting vessels
Bones or portions of bones that have limited collateral circulation and few vascular foramina are susceptible to avascular necrosis
is avascular necrosis considered a medical emergency
YES
any joint that is infected is considered a medical emergency
clinical manifestation of avascular necrosis
hip pain
antalgic gait
osteonecrosis of jaw (characterized by exposed bone in the mouth, numbness or heaviness in the jaw, pain, swelling, infection, and loose teeth (V3: inferior alveolar/mental nerve))
diagnosis of avascular necrosis
bone scar
mri
ct scans
pharmacology of avascular necrosis
depends on the severity
core decompression (early)
total joint replacement (late)
analgesics, NSAIDs
bisphosphonates (encourage bone growth)
PT intervention avascular necrosis
maintain WB status (protect it)
exercise to maintain ROM
essential to protect collapse of lesion
