4/18 SNSA - Corbett

Question 1

summary table of SNSAs

Answer 1

Question 2

seronegative spondyloarthropathies

break down terms

involved dieases

MSK features

genetic features

Answer 2

seronegative = NO rheumatoid factor

spondyloarthropathies = disease of SI joints and/or spine

four SYSTEMIC infl joint disorders (PAIR)

1. Psoriatic arthritis
2. Ankylosing spondylitis
3. Infl Bowel Disease-associated spondyloarthropathy
4. Reactive arthritis (aka Reiter’s syndrome)

*undifferentiated spondyloarthropathy

uniting clinical/radiographic/genetic features

• MSK features
  
  • infl of axial skeleton (spine and SI disease)
  • asymmetrical oligoarthritis
    
    • infl of four or fewer periph joints
  • marked extrasynovial infl
    
    • enthesis (sites of insertion of ligs/tends) + jt capsule, periosteum, cartilage, subchondral
    • dactylitis
• ​genetic features
  
  • HLA-B27 predisposition (esp in ankylosing spondylitis)
• extra-axial conds: ocular (uveitis), GI (IBD), GU, cardiac (aortitis, valvular insuff, heart block), cutaneous (keratoderma blennorhagicum)

Question 3

SNSA features: MSK fts

infl of axial skeleton

Answer 3

sx of “infl back pain”

• tenderness of SI joints by direct or indirect pressure
• limited spinal ROM (Schober test)
• deformity
  
  • loss of lumbar lordosis
  • accentuated thoracic kyphosis
• resolution of inflammation occurs by FIBROSIS
• periarticular osteitis and periostitis can result in bony syndesmophytes (bridge adj vertebral bodies, protrude at sites of lig attachment) → fusion of joint
  
  • new bone laid down instead of old bone eroded
  • “bamboo spine”

Question 4

SNSA features: MSK fts

oligoarthritis

Answer 4

oligo = 2-4 joints involved!

• mono: 1: septic arthritis, crystal arthropathy
• oligo: 2-4: SNSAs
  
  • typically involves lower extremities
• poly: 4+: RA

Question 5

SNSA features: MSK features

extrasynovial infl

Answer 5

infl outside of joint space

enthesitis: infl at fibrous points where ligs and tendons attach

• erosion and osteitis
• ossification
• periosteal new bone formation

*mostly lower extremities, but also axial spine (ex. Achilles)

Question 6

RA vs enthesitis of SNSA

Answer 6

RA: target is where the capsule is inserting onto bone

• osteoclasts consume the bone → erosion

SNSA enthesitis: target is outside bone space

• bone loss, but new bone made quickly

Question 7

dactylitis

Answer 7

“sausage digit”

most commonly assoc with psoriatic arthritis (all assoc with the other SNSAs)

flexor synovitis due to infl of tendon sheath

Question 8

skin lesions

ocular involvement

cardiac involvement

Answer 8

Question 9

treatment

Answer 9

1. relief of sx
2. aggressive strategy of disease mod: slow or stop disease progression, maintain/preserve fx
3. support patients/help cope

Question 10

ankylosing spondylitis

Answer 10

most common SA

“immobility and consolidation”

“infl of vertebrae”

1. axial skeleton (SI joints, spine)

2. male predominance (3-9x; white males 15-40yo)

3. 90% HLA B27 (5-6%)

dx often delayed

Question 11

when think ankylosing spondylitis?

red flags

Answer 11

• age under 40
• chronicity (insidious onset for longer than 3mo)
• infl back pain
  
  • sx worse in AM, inactivity → improve with exercise (not rest)

Question 12

when think mechanical process?

red flags

Answer 12

1. increasing age at onset
2. chronicity: acute onset (ex. while lifting), or chronic w/ OA
3. “mechanical”-type pain (radicular radiation, sx worse with activity)

Question 13

Schober test

Answer 13

assessment of spine mobility

Question 14

key clinical features of ankylosing spondylitis

(systemic)

what would you NOT expect?

Answer 14

enthesitis

peripheral arthritis

anterior uveitis

DONT EXPECT dactylitis (more common in psoriatic arthritis)

Question 15

key radiologic features of ankylosing spondylitis

Answer 15

Question 16

treatment of ankylosing spondylitis

Answer 16

1. NSAIDs (sx relief)
2. sulfasalazine (for peripheral jt disease - not effective for spondylitis)
3. TNFalpha antagonist

• adalimumab
• etanercept
• infliximab

Question 17

AS summary

Answer 17

Question 18

reactive arthritis

etiology

associated HLA

triad

Answer 18

inflammatory arthritis triggered by infectious agent outside joint

• oculogenital: Chlamydia
• enteric: Shigella, Salmonella, Campylobacter, Yersinia
• facultative intracellular pathogens

**arthritis is self perpetuating → NOT responsive to antibiotics!

• present 1-4wk after infectious event with asymmetric arthritis (LE oligoarth), enthesitis, dactylitis, sacroiliitis, spondylitis

TNF secretion is key to pathogenesis → acts as infl mediator in synovium, enthesis, and bone

• potentiates bone resorption by clasts

associated with HLA B27 (80% with ReA)

subset have triad: urethritis, uveitis, arthritis

• “can’t see, can’t pee, can’t climb a tree”

Question 19

ReA

non-articular features

Answer 19

Question 20

ReA treatment

Answer 20

most pts: ReA resolves in 4-6mo

30% recurrent/chronic sx

1. NSAIDs
2. sulfasalazine/MTX
3. TNFalpha antagonist

Question 21

ReA key points/summary

Answer 21

Question 22

psoriatic arthritis

Answer 22

20-30% of pts with psoriasis

HLA B27 and HLA Cw

pathophys

• T cell mediated
• TNF is an imp target

peripheral jt disease (95%)

• small joint polyarth
• asymmetrical oligoarthritis of LE
• dactylitis
• DIP arthropathy + nail pitting
• erosive arthritis

Question 23

Psoriatic arthritis vs RA?

Answer 23

Question 24

arthritis mutilans

Answer 24

5% of psoriatic arthritis

v severe

due to bone remodeling

“pencil in cup deformity”

Question 25

psoriatic arthritis key points/summary

Answer 25

Question 26

IBD-assoc spondyloarthropathy

Answer 26

HLA B27 assoc

20% of pt with IBD (more common w Crohn’s than UC)

asymmetric LE arthritis that tracks with GI disease

abrupt onset (type1)

Question 27

treatment of IBD spondyloarthropathy

Answer 27

1. NSAIDs
2. sulfasalazine/MTX
3. TNFalpha antags