seronegative arthritis

Question 1

ankylosing spondylitis

Answer 1

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

Question 2

ankylosing spondylitis etiology

Answer 2

about 90% of those with AS are HLA-B27 positive

human leukocytic antigen

Question 3

ankylosing spondylitis pathogenesis

Answer 3

marked by a chronic non granulomatous inflammation

Question 4

ankylosing spondylitis clinical manifestations

Answer 4

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

Question 5

ankylosing spondylitis diagnosis

Answer 5

MRI

short tau inversion, “Square sharpe vertebral column”

Question 6

ankylosing spondylitis treatment

Answer 6

NSAIDs

DMARDs

TNF-ALPHA (effective in preventing progression by decreasing activity, inflammation and improve spinal mobility)

Question 7

ankylosing spondylitis PT intervention

Answer 7

strengthen of trunk extensors = prevent flexion

exercise is very important

Question 8

Reiter’s syndrome

Answer 8

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

Question 9

what are the most common microbial pathogens of reiter’s syndrome

Answer 9

shigella

salmonella

yersinia

campylobacter

chlamydia

Question 10

who is affected the most by reiter’s syndrome

Answer 10

men in their 30s

Question 11

classical triad of symptoms reiter’s disease

Answer 11

urethritis

conjunctivitis

arthritis

combination of peripheral arthritis w/ urthritis lasting long that 1 month is necessary before the diagnosis can be confirmed

Question 12

treatment of reiter’s syndrome

Answer 12

NSAIDs

Question 13

psoriatic arthritis

Answer 13

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

Question 14

when does psoriatic arthritis present

Answer 14

during the 2nd and 3rd decades of life

w/ onset of the arthritis occurring up to 20 years later

Question 15

psoriatic arthritis pathogenesis

Answer 15

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

Question 16

psoriatic arthritis clinical manifestations

Answer 16

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

Question 17

PT intervention for psoriatic arthritis

Answer 17

maintain mobility, pain control, decrease amount of joint damage

Question 18

osteoarthritis

Answer 18

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

Question 19

primary OA

Answer 19

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

Question 20

secondary OA

Answer 20

has a known cause, which may be trauma, infection, hemarthrosis, osteonecrosis

Question 21

OA etiology & risk factors

Answer 21

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

Question 22

OA pathogenesis

Answer 22

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

Question 23

OA clinical manifestations

Answer 23

Bony enlargement, limited range of motion, crepitus on motion

Characteristic Hand Deformities

Heberden’s Nodes: DIP

Bouchard’s Nodes: PIP

Question 24

OA pharmacology

Answer 24

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

Question 25

OA PT intervention

Answer 25

manual pt and supervised exercise

instruct body mechanics

ice per mild swelling

aquatic therapy

Question 26

neurogenic arthropathy

Answer 26

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

Question 27

avascular necrosis

Answer 27

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

Question 28

what does necrosis result from

Answer 28

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

Question 29

is avascular necrosis considered a medical emergency

Answer 29

YES

any joint that is infected is considered a medical emergency

Question 30

clinical manifestation of avascular necrosis

Answer 30

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))

Question 31

diagnosis of avascular necrosis

Answer 31

bone scar

mri

ct scans

Question 32

pharmacology of avascular necrosis

Answer 32

depends on the severity

core decompression (early)

total joint replacement (late)

analgesics, NSAIDs

bisphosphonates (encourage bone growth)

Question 33

PT intervention avascular necrosis

Answer 33

maintain WB status (protect it)

exercise to maintain ROM

essential to protect collapse of lesion