228. Spondyloarthropathies

Question 1

General characteristics of seronegative sphondyloarthropathies

Answer 1

1. negative RF (seronegative)
2. spine involvement/asymmetric joint involvement/enthesitis
3. absence of female predominance
4. therapy driven by disease manifestations MORE THAN specific diagnosis!!!!!
5. HLA B27+

Question 2

Reactive Arthritis (Epidemiology, Pathogenesis)

Answer 2

Acute inflammatory arthritis following GI/GU infection
M>W, self limited, but can be recurrent/chronic

Genetric Predispostion: HLA-B27+ (MHC I antigen presenting protein)
Environmental Trigger: Enteric Infection (Shigella, Salmonella, etc), Urogenital Infection (Chlamydia), may be asx!
Molecular Mimicry: sequence homology b/w HLA-B27 self and bacteria non-self antigens = auto-antibody response

Question 3

Reactive arthritis (Features)

Answer 3

Additive asymmetric mono/oligo arthritis in large lower extremity joints
Dactylitis: diffusely swollen joints
Enthesitis: at heel of achilles, subchondral bone inflammation/resoprtion, periosteal new bone formation (bone spurs)
Inflammatory low back pain
Skin: Psoriasis-like scaly discrete plaques
Musoca: Painless oral ulcers
Nails: thickened and opacified
Eyes: Conjuctivitis/Uveitis

Question 4

Reactive Arthritis (Treatment)

Answer 4

NOT ABx - microbes are gone, but the auto-antibody reaction has persisted

Need anti-inflammatory agents (NSAIDs), PT

If NSAIDs fail: corticosteriods, DMARDs/biologis if severe

Question 5

Psoriatic Arthritis (PsA) 
(Epidemiology)

Answer 5

Psoriasis common: 2-3% population, peak onset in late teens/early 20s
PsA in 5-39% pts with psoriasis
M = F
PsA develops 10 years after psoriasis (peaks late 20s/early 30s)

Question 6

PsA Clinical Features

Answer 6

Cutaneous: Psoriatic Plaques, Onycholysis/Nail pitting, Guttate/Pustular Variants
Polyarthritis: Inflammatory, DIPs! (RA is PIP/MCP), and Axial
Dactylitis
Enthesitis
Arthritis Mutilans- telescoping of digits
Destructive Arthritis: joints eaten away - productive erosions “pencil in cup” pathognomonic for PsA

ONLY Arthritis with destructive (pencil) AND productive bone changes (cup)

Question 7

PsA treatment

Answer 7

NSAIDs, corticosteriods
DMARDs (Sulfasalazine, MTX)

Next gen tx: PDE4-i’s (apremilast), JAK-i’s (Tofacitinib), TNFa-i’s (stop damage, not skin disease, don’t stop new bond formation)

No ideal first line treatment because we don’t know which patients will develop severe disease

Question 8

Axial Spondyloarthritis (AS)
(Epidemiology, Sx)

Answer 8

Sx begin in 20s (purely spine disease)

Inflammatory back pain/stiffness (worse in morning/better with activity)
Sacroilitis (White sclerosis around spine/pelvis = bone thickening)
Oligoarthritis
Enthesitis
Systemic (fatigue, impaired sleep)
Uveitis, IBD, aortitis (aortic root damage)

Question 9

AS imaging findings and dx criteria

Answer 9

Squaring and straightening of lumbar lordosis
Syndesmophytes: new bone bridges across spinous processes and inflammation = reduced mobility

DX: Sacroilitis + any clinical criteria

Question 10

AS tx

Answer 10

Exercise/PT (maintain spinal mobility)
NSAIDs, Corticosteroids, Sulfasalazine (Sx management)
MTX, TNFa-i’s - can IMPROVE mobility
IL-17-i’s

NSAIDS are FIRST LINE

Question 11

IBD related arthritis (sx, types)

Answer 11

Inflammatory Back Pain/Stiffness
Sacroilitis, Oligoarthritis, Enthesitis, Dactylitis, Systemic (Fatigue/Sleep), Change in bowel habits)
M = F

Type 1: Acute and Remitting (flares with IBD), pauciarticular, large joints
Type 2: Chronic Polyarticular Arthritis - symmetrical involvement of hands, independent of IBD
non-erosive arthritis May present before bowel disease (Chron’s or IBD)