Twenty Eight Flashcards
What are some characteristics that seronegative spondyloarthropathies share in common?
A. Group of joint disorders characterized by
1 . Lack of rheumatoid factor
2. Axial skeleton involvement
J. HLA-B27 association
-Peripheral arthritis – lower limb, asymmetric
-Radiographic sacroiliitis
-No SQ nodules or extra-articular RA features
-Overlapping extra-articular features (i.e. anterior uveitis)
-Significant familial aggregation
-Enthesitis – inflammation of site where tendon, ligament, capsule or fascia inserts into bone
What are SNSAs?
Ankylosing spondylitis (AS)
Reactive arthritis
Arthropathy of IBD (Crohn’s/UC)
Psoriatic arthritis
Undifferentiated spondyloarthropathy
Juvenile onset AS
What is ankylosing spondylitis? What joints are involved? Epidemiology? Presentation? Extra-articular manifestations?
B, Ankylosing spondylarthriti s involves the sacroiliac joints and spine.
1 . Arises in young adults, most often male
2. Presents with low back pain; involvement of vertebral bodies eventually arises, leading to fusion of the vertebrae (‘bamboo spine ).
3 . Extra-articular manifestations include uveitis and aortitis (leading to aortic regurgitation)
What physical exam findings are there in AS? Lab/imaging findings?
- Schober test – test of back flexion
- Reduced chest expansion
- Level of 4th ICS or just below breasts in female
- Pt. exerts maximal forced expiration followed by maximal inspiration - usually >5cm
- Less than 5cm is abnormal
- Evaluate for sacroiliitis – negative either very early or very late
- C-spine -patient stands erect against wall, extends neck to touch wall
- Normals can touch wall with occiput
•Distance between occiput and wall is degree of cervical
deformity
- Labs are nonspecific
- 95% of patients with AS are +HLA-B27 but no value in routine screening
- Elevated ESR in up to 75% of AS patients
- First x-ray changes usually in SI joints but may be negative in early disease and may only be evident on CT or MRI
- Classic XR is bamboo spine
What is the goal of AS treatment? Non-pharmalogical treatment? Pharmacological?
maximize long term health-related quality of life through control of symptoms and inflammation, prevention of progressive structural damage, preservation/normalization of function and social participation.
Non-pharmacological treatment
The cornerstone of non-pharmacological treatment of patients with AS is patient education and regular exercise.
Home exercises are effective. Physical therapy with supervised exercises, land or water based, individually or in a group, should be preferred as these are more effective than home exercises.
Patient associations and self-help groups may be useful.
Non-steroidal anti-inflammatory drugs
•NSAID are recommended as first-line drug treatment for AS patients with pain and stiffness.
Glucocorticoids
Corticosteroid injections directed to the local site of musculoskeletal inflammation may be considered.
Anti-TNF therapy
Anti-TNF therapy should be given to patients with persistently high
disease activity despite conventional treatments according to the ASAS
recommendations.
There is no evidence to support the obligatory use of DMARD before or
concomitant with anti-TNF therapy in patients with axial disease.
Surgery
Total hip arthroplasty should be considered in patients with refractory pain
or disability and radiographic evidence of structural damage, independent of
age.
Spinal corrective osteotomy may be considered in patients with severe disabling deformity.
In patients with AS and an acute vertebral fracture a spinal surgeon should be consulted.
What is reactive arthritis? What joints does it affect usually?
Reactive Arthritis
(preferred name over Reiter’s)
- Reiter’s syndrome = triad of arthritis, conjunctivitis, urethritis
- Arthritis 1-3 weeks after venereal infections (Chylamydia trachomatis) or gastroenteritis (Shigella flexneri, Salmonella typhimurium, Salmonella enteritidis, Yersinia enterocolitica, Yersinia pseudotuberculosis, Campylobacter jejuni to name a few)
- Mild constitutional symptoms, low grade fever but can appear toxic (high fever, weight loss, malaise)
- Arthritis typically LE (ankles, knees, feet) in asymmetric distribution, additive, can be after the eye or GU symptoms resolved
Lab findings in reactive arthritis?
Labs
- Mild normochromic, normochromic anemia
- Elevated ESR and CRP, complements
- RF and ANA negative
- Inflammatory synovial fluid
- Look for infection – stool culture, GU swab, and urine culture – but can be negative by time of arthritis
Treatment of reactive arthritis?
Treatment
- NSAIDs
- Local steroid injections
- Skin lesions – MTX, retinoids, phototherapy
- Eye – topical steroids, mydriatics, cycloplegics
- SSZ for peripheral arthritis
- TNF blockers
What is psoriatic arthritis? Joints affected?
D. Psoriatic arthritis is seen in 10% of cases of psoriasis.
1 . Involves axial and peripheral joints; DIP joints of the hands and feet are most commonly affected, leading to “sausage” fingers or toes.
•Constitutional symptoms are uncommon
What lab findings are there in psoriatic arthritis? Imaging?
–RF negative (actually RF+ 5-16% of pts and ANA + in 2-16% of pts)
–Elevated ESR
–Elevated uric acid
–Diagnosis is clinical – look for hidden psoriasis
Imaging
•XR changes early in the course suggest very aggressive disease or present
for longer duration
- Erosive changes and new bone at distal joints, pencil in cup
- Unilateral sacroiliitis
- C-spine involvement
- Bony spurs/periosteal reaction
- Marginal syndesmophytes
Treatment of psoriatic arthritis?
Treatment
- NSAIDs + topicals
- MTX – for skin and joint
- Sulfasalazine – 44% don’t tolerate side effects
- TNF blockers
What is enteropathic arthritis? Pattern of arthritis/joints involved? Other manifestations?
Enteropathic Arthritis
- Inflammatory bowel disease-Crohn’s and Ulcerative colitis(UC) – different disease but similar arthritis
- Axial – 10-20% cases, similar to AS, symptoms of spinal involvement do not vary with intestinal disease activity
- Note: In IBD related AS - +HLA-B27 in 50-70%
- Peripheral Joint – MCP, PIP, knees, ankles – Crohn’s >UC, typically non-destructive, reversible but can get erosions
- Note: Symptoms coincide with gut activity – total colectomy associated with arthritis remission in 1⁄2 of pts with UC, although arthritis can begin post-surgery
- Other manifestations include
–Clubbing
–Uveitis – can be bilateral and chronic
–Skin – pyoderma gangrenosum
What is infectious arthritis? What microbes cause it? Joint location? Presentation?
V. INFECTIOUS ARTHRITI S
A. Arthritis due to an infectious agent, usually bacterial
B. Causes include
1. N goriorrh oeae—young adults most common cause
2. S aureus— older children and adults; 2nd most commo n cause
C. Classically involves a single joint, usually the knee
D. Presents as a warm joint with limited range of motion; fever, increased white count, and elevated ESR are often present,
What is the pathophysiology of gout? What is the etiology of primary gout? What are some etiologies of secondary gout? Which is more common?
A. Deposition of monosodium urate (MSU) crystals in tissues, especially the joints
B. Due to hyperuricemia; related to overproduction or decreased excretion of uric acid
1 . Uric acid is derived from purine metabolism and is excreted by the kidney.
C. Primary gout is the most common form; etiology of hyperuricemia is unknown.
D. Secondary gout is seen with
1 . Leukemia and myeloproliferative disorders—Increased cell turnover leads to
hyperuricemia.
2. Lesch-Nyhan syndrome—X-linked deficiency of hypoxanthine-guanine
phosphoribosyltransferase (HGPRT); presents with mental retardation and selfmutilation
3 . Renal insufficiency—decreased renal excretion of uric acid
How does gout present? What triggers this? What does chronic gout lead to? How?
E. Presents as exquisitely painful arthritis of the great toe (podagra)
1 . MSU crystals deposit in the joint, triggering an acute inflammatory reaction.
2. Alcohol or consumption of meat may precipitate arthritis.
F. Chronic gout leads to
1 . Development of tophi—white, chalky aggregates of uric acid crystals with
fibrosis and giant cell reaction in the soft tissue and joints (Fig. 18,9A)
2. Renal failure—Urate crystals may deposit in kidney tubules (urate nephropathy)
