Seronegative Spondyloarthropathies Flashcards Preview

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Flashcards in Seronegative Spondyloarthropathies Deck (60):

What are the (seronegative) SPONDYLOARTHROPATHIES?

–Ankylosing spondylitis (AS)

–Enteropathic arthritis (inflammatory bowel disease-associated arthropathy)

–Reactive arthritis (Reiter’s syndrome)

–Psoriatic arthritis

–Undifferentiated Spondyloarthropathies

–Juvenile chronic arthritis and Juvenile –Onset Ankylosing Spondylitis


What are some of the commonalities of spondyloarthropathies?

-RF negative

-significant familial aggregation

-axial skeletal involvement with sacroilitis and spondylitis 

-Large-joint asymmetric oligoarthritis predominantly lower extremities


-no RA nodules 


What HLA type are spondyloarthropathies associated with?

HLA-B27 (an MHC class I molecule that binds antigenic peptides and presents them to CD8+ T cells)

present in over 90% of AS patients but only 8% of normal population

present in 75% of reactive arthritis (Reiter's) patients



Common 'itis'-es of spondyloarthropies?

-sacroilities (sacrum)

-spondylitis (spine)

-enthesitis (tendon, ligment)-top

-dactylitis (digits)-bottom

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Patients with psoriasis or IBD that are HLA-B27 positive are more likely to develop ______.

axial (spinal) arthropathy


What is the patient population for Ankylosing spondylitis (AS)?

adeolscence to age 35 when a MALE predominance (3:1)


What is the pathology of AS?

There is inflammatory cell infiltrate with synovial inflammation similar to RA and TNFa excess (ANTI-TNF AGENTS GREAT FOR THIS)


How does AS present?

classic clinical features of symmetrical sacroilitis and spondylitis that present insidiously as chronic lower back pain and stiffness that are *worse in the morning and improve with exercise* and gradually ascend up the spine


Is peripheral joint involvement common in AS?

It can be seen in up to 1/3 of patients and typically involves hips, shoulders, knees, and ankles and is usually asymmetric 

dactylitis and enthesisits (achiless or plantar most common) can occur

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What is going on here in this patient with AS?

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There is inflammation of the spinal joints causing bony fusion of the spine and a decreased range of motion


How does AS present upon exam?

1.Sacroiliac tenderness

2.Limited spine range of motion in all directions

3.Loss of lumbar lordosis, thoracic and cervical kyphosis

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What is Schober's test for AS?

Find the PSISs, mark the center point between the two, mark 5 cm below and 10 cm above this point. Then ask the patient to bend over with knees forward and attempt to touch toes. A change in the distance between the bottom and top mark of greater than 4-5cm is normal. Less than 3cm increase raises suspicion of AS


What is a chest expansion test for AS?

Find the 4th intercostal space, then ask patients to put hands behind head, then measure the circumference of the chest thenask the patient to breath in and you want to see an increase of greater than 2.5cm 


What is going on here?

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•Sacroiliitis (usually bilateral)- typical in AS


What processes are occuring here?

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Left: squaring of the vertebral bodies

Right: Syndesmophyte formation 

in AS


What are some common extra-articular features of AS?

Anteriot uveitis can be seen in up to 30% of patients, as well as aortic regurg and heart block and lung fibrosis or thoracic cage restriction 


Aortic regurgitation and heart block 2x more common in AS if patient has what?

peripheral joint involvement


What is this?

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Anterior uveitis seen in AS


Treatment of AS?

First to last:

-NSAIDs, then Sulfasalazine (if peripheral involvement), then Local steroids, then TNFa blockers (Humira)

analgesics and physical therapy throughout

and eventually surgery if needed 

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What is reactive arthritis?

Inflammatory arthritis arising after an infectious process that presents with the classic triad of:




"cant see, cant pee, cant bend my knee"

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What are some common GI pathogens assoicated with Reactive Arthritis?



-Yersinia enterocolitica(not plague)

-Shigella or Clostridium difficile 


What are some common GU pathogens assoicated with Reactive Arthritis?

-Chlamydia trachomatis

-Mycoplasma species (maybe)


What are some common Respiratory pathogens assoicated with Reactive Arthritis?

Chlamydia pneumoniae 


Patient Population for Reactive Arthritis?

This is a very uncommon disease that favors MALEs and is more common (and more severe) in HIV/AIDS patients 


Elvis had this shit 

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HLA type for Reactive Arthritis?



Clinical features of interest in reactive arthritis besides the classic triad:

-arthritis may present as asymmetric oligoarthritis

-oral ulcerations


-Keratoderma blennorrhagica 

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What is this?

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•Circinate balanitis seen in reactive arthritis 


What is this?

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•Nails - onycholysis seen in reactive arthritis (the painless separation of the nail from the nail bed)


What is this?

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•Keratoderma blennorrhagica seen in reactive arthritis 


Lab tests for reactive arthritis?

•Inflammatory markers (ESR, CRP)

•Culture (unusual to be +) or Serology for potential pathogens if indicated

•Consider HIV

•HLA B27


How long does reactive arthritis typically last?


•Mean duration of 2 to 3 months

•Recurrences are common

•20% to 50% of patients demonstrate a chronic course


make sure to follow up for observation


What is psoriatic arthritis?

Psoriatic arthritis is a progressive disease, with 47% of patients developing erosions within 2 years of diagnosis. Psoriatic arthritis should be suspected in a patient with an asymmetric joint distribution pattern who may have additional clinical features, such as dactylitis, enthesitis, or inflammatory-type back pain, and who is negative for rheumatoid factor.

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What are the markers for poor outcome in PA?

Polyarticular disease and an elevated erythrocyte sedimentation rate (ESR)


Way to distinguish PA from rheumatoid arthritis?

1.Studies of synovial tissue have highlighted an increase in vascularity and the presence of neutrophils as helping to distinguish spondyloarthropathy from rheumatoid arthritis. Change in synovial CD3+ T cell infiltration might correlate with clinical response to treatment.

2. Prominent entheseal involvement with bone marrow edema at entheseal insertions on magnetic resonance imaging has prompted the hypothesis that psoriatic arthritis may originate at the enthesis.

3. A role for CD8+ T cells and the innate immune response has been proposed.


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Fibroblasts from skin and synovium proliferate and secrete IL-1, IL-6, and PDGF


Other than skin psoriasis, what is a very common manifestation of PA?

Nail dystrophic changes. A, Nail pitting; B, onycholysis; and C, severe destructive change with nail loss and pustule formation.

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How does the Synovial cytokine profile compare to that of RA?

Very similar BUT:

–More TNF-alpha, IL-1 beta, IL-2, IL-10, and INF gamma

–Less IL-4


PsA synovium has less lining layer thickness and more vascularity


What serum cytokines are uprgulated in PsA?






–Fibroblast Growth Factor


One unique thing seen in serum and synovial tissue in PsA is increased IL-18. What is the effect of this?

–Stimulates angiogenesis

–Upregulates chemokine expression on synovial fibroblasts

–Increases mononuclear cell recruitment


What is this?

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Arthritis Mutilans pattern of PsA (one of several patterns)


What is this?

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•DIP involvement

•“Pencil – in - a – cup” appearance on x-ray in PsA


In PsA, Patients treated with _____ experience clinically significant improvements in skin lesions.


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What is enteropathic arthritis?

•Inflammatory arthritis associated with

–Crohn’s disease

–Ulcerative colitis

–Whipple’s disease (rare)

that occurs in 2% to 20% of patients with IBD

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What type of eneropathic arthritis is associated with HLA B27?

•Axial disease (not peripheral arthritis) 

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T or F. Enteropthic arthritis usually occurs AFTER onset of GI disease



What is this?

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How is enteropathic arthritis treated?

1.Symptomatic treatment is often adequate and NSAIDS, although a potential problem causing flares of IBD, are often well tolerated and effective for spine involvement or enthesitis.

2.Sulfasalazine and its derivative 5-acetysalicyylic acid (5-ASA) inhibit NFk B and have shown efficacy in UC but not CD.

3.Glucosteroids are effective in both UC and CD, local joint injection is effective in oligoarthritis of IBD.

4.Azathioprine and methotrexate are effective in both forms of IBD.

5.Infliximab and adalimumab are effective in CD and Infliximab is effective in UC.



CeD is caused by an immune reaction to partly digested wheat gluten by T lymphocytes in the gut of genetically HLA-DQ2-positive or HLA-DQ8-positive individuals

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Common symptoms of CeD?

2/3 of patients with CeD present with diarrhea or irritated bowel symptoms, and fatigue, headache, and arthralgias are common


The primary findings of mucosal inflammation, crypt hyperplasia, and villous atrophy can result in marked degrees of malabsorption. This can result in weight loss, growth retardation in children, anemia, and vitamin deficiencies particularly of the B and D groups. Thus, osteoma­lacia can develop.


Less common symptoms of CeD?

25% are associated with development of type I diabetes, anemia, osteoporosis (lack fo vitD absorption), and neuropathies.


Affected patients may present with diffuse achiness and bone pain, which is most prominent in the lower spine, pelvis, and legs.


How is CeD diagnosed?

Diagnosis is widely small bowel biopsy, and presence of serum IgA antitissue transglutaninase and IgA antiedomysial antibodies.


How is CeD treated?

Treatment is to eliminate gluten from the diet.


What the fuck is gluten anyways?

Celiac disease or gluten enteropathy is an inflammatory disorder of the proximal small intestine triggered by the ingestion of gluten, the alcohol-soluble fraction of wheat protein.


An association between _______ deficiency and celiac disease has been well established.

selective lgA


Approximately 10 per­ cent of patients with IgA deficiency have been found to have celiac disease.


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See normal glands (circles) - they should be close together. If they are not, suspect inflammation or fibrosis (like in here)


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Increase in size of the epidermis with too much keratin on the suface (second layer of light pink, right)

perikeritosis- nuclei remain in the keratin debris (top layer of pink, right)

with Monro-microabscesses (composed of neutrophils)- right under the second pink layer on the right 

capillary loop dilation seen as well 


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Left: normal colon and 'cigarette' package appearance right next to it 

inflammation in the gut can be NORMAL 

right- these are full of neutrophils (aka active inflammation)- active cryptitis 

bottom right- need to see architectural distortion to call something IBD (loss of test tube shape)





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On right because the thoracic aorta prevents it from occurring on the left 


Patients with psoriasis or IBD that are HLA-B27 positive are more likely to develop what?

axial (spinal) arthropathy