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Rheumatology > Psoriatic Arthritis and Axial Spondyloarthritis > Flashcards

Psoriatic Arthritis and Axial Spondyloarthritis Flashcards

1
Q

What are spondyloarthropathies?

A

A group of related inflammatory musculoskeletal diseases that show overlap in their clinical features and have a shared immunogenic association with HLA-B27.

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2
Q

What are some examples of spondyloarthropathies?

A

Axial spondyloarthritis
Ankylosing spondylitis
Reactive arthritis
Psoriatic arthritis
Arthritis with IBD (enteropathic spondyloarthritis)

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3
Q

In what spondyloarthropathies is the axial skeleton predominantly affected?

A

Axial spondylitis and ankylosing spondylitis

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4
Q

How do SpAs contrast to RA?

A

In SpAs there are frequent and notable non-synovial musculoskeletal lesions - mainly inflammatory in nature - of ligaments, tendons, periosteum and other bone lesions.

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5
Q

What is a hallmark lesion of all SpAs?

A

Enthesitis (also possibly dactylitis)

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6
Q

What is enthesitis?

A

Inflammation at the site of a ligament or tendon insertion into bone

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7
Q

What is dactylitis?

A

Inflammation of a whole finger or toe

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8
Q

Why are SpAs thought to arise?

A

As the result of an abherrent host response to infection and abnormal mucosal immunity mediated through changes in the IL12, IL-23 and Th17 axis.

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9
Q

What are the triggering organisms in reactive arthritis?

A

Bacterial dysentery or chlamydial urethritis

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10
Q

Do SpAs run in families?

A

Yes, it is not only common to the specific condition but may extend to other diseases in the spondyloarthropathy group.

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11
Q

What are the axial spondyloarthropathies?

A

Ankylosing spondylitis (AS) as well as axial spondyloarthritis (axSpA)

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12
Q

What are the characteristic features of axSpA?

A
  • Inflammatory changes in the entire axial skeleton (and can be visualized on MRI)
  • Structural alterations, such as new bone formation with syndesmophytes and ankylosis, develop later in the course of the disease.
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13
Q

What is axial spondyloarthritis diagnosed from?

A

Sacrolitis on MRI + one other feature on history, clinical examination or investigation. (the diagnosis can be made in HLA-B27-positive patients with >1 clinical feature in the absence of sacrolitis).

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14
Q

What is ankylosing spondylitis diagnosed from?

A

Can be diagnosed on X-ray evidence of sacrolitis with one other feature on history or examination.

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15
Q

What is sacrolitis?

A

Sacroiliitis is an inflammation of the sacroiliac joint, which is located on either side of the low back where the spine joins the hips (pelvic bones). Sacroiliitis can occur on one or both sides. Symptoms include pain in the buttocks or low back that can spread down the leg.

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16
Q

What is the difference seen on imaging between AS and axSpA?

A

axSpA: Sacrolitis on MRI only
AS: Bilateral sacrolitis on X-ray, even if changes are mild OR unilateral sacrolitis on X-ray if changes are definite.

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17
Q

What are features of axSpA discovered in the history?

A
  • Back pain >3 months that has four of the following characteristics:
    1 improved by exercise
    2 not relieved by rest
    3 insidious onset
    4 night pain
    5 age at onset <45
  • Good response of back pain to NSAID
  • FH of spondylarthritis
  • History of IBD
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18
Q

What are the features of AS discovered in the history?

A

Low back pain >3 months improved by exercise and not relieved by rest.

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19
Q

What may you find on clinical examination in someone with axSpA?

A
  • Arthritis
  • Enthesitis
  • Uveitis
  • Dactylitis
  • Psoriasis
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20
Q

What may you find on clinical examination in someone with AS?

A
  • Limitation of lumbar spine movement in sagittal and frontal planes
  • Chest expansion is reduced
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21
Q

What may you find from investigations in axSpA?

A

HLA-B27 positive
Elevated CRP

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22
Q

What are the clinical features of axSpA?

A
  • Cardinal feature is inflammatory back pain and early morning stiffness, with low back pain radiating to the buttocks or posterior thighs if the sacroiliac joints are involved
  • Symptoms are exacerbated by inactivity and relieved by movement
  • Musculoskeletal symptoms may be prominent at entheses, may be episodic and if persistent, can present as widespread pain and be mistaken for fibromyalgia.
  • Fatigue is common
  • History of psoriasis (current, previous or in first degree relative) and inflammatory bowel symptoms (current or previous) are important clues.
  • A reduced range of lumbar spine movements in all directions
  • Pain on sacroiliac stressing and a high enthesitis index.
  • Entheses that are typically affected are Achilles’ insertion, plantar fascia origin, patellar ligament entheses, gluteus medius insertion at the greater trochanter and tendon attachments at humeral epicondyles
  • Aortic regurgitation
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23
Q

What validated clinical questionnaire can be used to aid diagnosis of axSpA?

A

Assessment of Spondyloarthritis International Society Health Index (ASAS-H)

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24
Q

What investigations should be undertaken to aid diaagnosis of axSpA?

A

Ultrasound or MRI or entheses
Or MRI of the sacroiliac joints and spine.
- Other findings may include raised ESR and CRP (though these may be normal)
- Anaemia
- Positive HLA-B27
- Faecal calprotectin is a useful screening test for associated IBD.

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25
Q

How is axSpA treated at outset?

A
  • At outset patient education, NSAID use and physical therapy are key interventions
26
Q

How is axSpA treated in cases of severe and/or persistent peripheral musculoskeletal features?

A

Both sulfasalazine and methotrexate are reasonable choices.

27
Q

In patients who fail to respond adequately or who cannot tolerate NSAIDs, what treatment should be used?

A

Biologic therapy with either TNF inhibitors or the IL-7A inhibitor secukinumab should be considered.

28
Q

What is the prognosis of axSpA?

A

HLA-B27 positivity, high persistent CRP and high functional incapacity are likely to be markers of poor prognosis, if not markers of extension to AS.

29
Q

How is Ankylosing spondylitis defined?

A

By the presence of sacroilitis on X-ray and other structural changes on spine X-rays, which may eventually progress to bony fusion of the spine.

30
Q

What is the male to female ratio of those suffering with Ankylosing Spondylitis?

A

male:female 3:1

31
Q

What are the clinical features of Ankylosing Spondylitis?

A
  • Same as in axSpA
  • AS typically evolves slowly, with fluctuating symptoms of spinal inflammation; ankylosis develops in many patients over a period of many years.
  • Secondary osteoporosis of the vertebral bodies frequently occurs, leading to an increased risk of vertebral fracture.
  • Spinal fusion occurs and this may lead to kyphosis of dorsal and cervical spine - may be incapacitating especially when associated with fixed flexion contractures of the hips or knees.
  • 40% of patients have peripheral musculoskeletal lesions (asymmetrical, affecting entheses of large joints, such as hips, knees, ankles and shoulders)
  • Fatigue is major complaint
  • Acute anterior uveitis is moost common extra-articular feature, which occasionally precedes joint disease.
32
Q

What investigations should be undertaken to aid diagnosis of AS?

A
  • X-ray of sacroiliac joint show irregularity and loss of cortical margins, widening of the joint space and subsequently sclerosis, joint space narrowing and fusion.
  • Lateral thoracolumbar spine X-rays may show anterior ‘Squaring’ of the vertebrae due to erosion and sclerosis of the anterior corners and periostitis of the waist
  • Bridging syndesmophytes may also be seen
  • In advanced disease, ossification of the anterior longitudinal ligament and facet joint fusion may also be visible.
  • Combination of these features may result in a typical bamboo spie.
  • erosive changes may be seen in the symphysis pubis, ischial tuberosities and peripheral joints.
  • DXA scanning due to osteoporosis association
  • ESR and CRP are raised in active disease but may be normal; anaemia is often present.
  • Autoantibodies such as RF, ACPA and ANA are negative.
33
Q

-How is Ankylosing Spondylitis treated/managed?

A
  • Mobilising exercises are important
  • Long acting NSAID at night is helpful for alleviation of morning stiffness
  • Anti-TNF or anti-IL-17A therapy should be considered in patients who are inadequately controlled on standard therapy, as described for axSpA
  • Local glucocorticoid injections can be useful for persistent plantar fascitis, other enthesopathies and peripheral arthritis
  • Oral glucocorticoids may be required for acute uveitis
  • Severe hip, knee or shoulder arthritis with secondary OA may require arthroplasty
  • Spinal osteotomy can make significant difference to patients with severe ankylosed kyphotic spines.
34
Q

What are bridging syndesmophytes?

A

Areas of calcification that follow the outermost fibres of the annulus

35
Q

What is reactive (spondylo)arthritis ReA?

A

A reaction to a number of bacterial triggers with clinical features in keeping with all SpA conditions.

36
Q

What are the known triggers of reactive arthritis?

A

Chlamydia, Campylobacter, Salmonella, Shigella and Yersinia.

37
Q

What is sexually acquired reactive arthritis (SARA)?

A

A disease of young men (predominantly) with a male preponderance of 15:1. - meaning it is hard to detect in women especially as they are asymptomatic with chlamydia.

38
Q

What are the clinical features of Reactive arthritis?

A
  • Typically acute onset
  • Presents with an inflammatory enthesitis, oligoarthritis and/or spinal inflammation
  • Lower limb joints and entheses are predominantly affected.
  • In all types of ReA, there may be considerable systemic disturbance, with fever and weight loss.
  • Achilles insertional enthesitis/tendonitis or plantar fasciitis may also be present.
  • The first attack of arthritis is usually self-limiting but recurrent or chronic arthritis can develop and about 10% still have active disease 20 years after the initial presentation.
  • Low back pain and stiffness due to enthesistis and osteitis are common and 15-20% of patients develop sacrolilitis.
  • Many extra-articular features of ReA involve the skin, especially in SARA
  • Other complications are rare but include aortic incompetence, conduction defects, pleuro-pericarditis, peripheral neuropathy, seizures and meningoencephalitis.
39
Q

What are the extra-articular features of ReA?

A
  • Circinate balanitis (starts as vesicles on the coronal margin of the prepuce and glans penis, later rupturing to form superficial erosions with minimal surrounding erythema, some coalescing to give a circular pattern.)
  • Keratoderma blennorrhagica which begins as discrete, waxy, yellow-brown vesico papules with desquamating margins, occasionally coalescing to form large crusty plaques on the palms and soles of feet.
  • Pustular psoriasis
  • Nail dystrophy with subungual hyperkeratosis
  • Mouth ulcers
  • Conjunctivitis
  • Uveitis (rare with first attack but arises in 30% of patients with recurring or chronic arthritis)
40
Q

What investigations should be performed to aid diagnosis of reactive arthritis?

A
  • Diagnosis made clinically normally
  • Joint aspiration may be required to exclude crystal arthritis and articular infection
  • ESR and CRP raised
  • Urethritis may be confirmed in 2 glass test
  • High vaginal swabs to test for chlamydia
  • Stool sample usually negative by onset of symptoms (except in post-salmonella arthritis)
  • Serology may confirm previous dysentery
  • RF, ANA and ACPA all negative
  • in chronic/ recurrent disease, X-ray show periarticular osteoporosis; proliferative erosions, notably at entheses; periostitis, especially of metatarsals, phalanges and pelvis; and large fluffy calcaneal spurs.
  • In contrast to AS, radiographic sacroilitis is often asymmetrical and often unilateral and syndesmophytes are predominantly coarse and asymmetrical, often extending beyond the contours of the annulus.
  • Radiographic changes in the peripheral joints and spine identical to those seen in psoriasis
41
Q

What is the treatment/management of reactive arthritis?

A
  • Should be treated with rest, NSAIDs and analgesics.
  • Intra-articular or systemic glucocorticoids may be required in patients with severe monarticular synovitis or polyarticular disease, respectively.
  • No convincing use for antibiotics unless triggering infection is identified.
  • If chlamydial urethritis is diagnosed, it should be treated empirically with a short course of doxycycline or single dose of azithromycin
  • Treatment with DMARDs (usually sulfasalazine or methotrexate) should be considered for patients with persistent marked symptoms, recurrent arthritis or severe keratoderma blennorrhagia.
  • Anterior uveitis is a medical emergency requiring topical, subconjunctival or systemic glucocorticoids.
  • For DMARD-recalcitrant cases, anti-TNF therapy should be considered
42
Q

What is the prevalence of psoriatic arthritis in patients with psoriasis?

A

40%

43
Q

What is the age of onset of psoriatic arthritis?

A

Between 25 and 40 but juvenile forms exist.

44
Q

What are the CASPAR criteria for psoriatic arthritis?

A

Inflammatory articular disease (joint, spine or enthesis) with >= 3 point from the following:
- Current psoriasis (2)
- History of psoriasis in first or second degree relative
- Psoriatic nail dystrophy
- Negative IgM rheumatoid factor
- Current dactylitis
- History of dactylitis
- Juxta-articular new bone

45
Q

What is the pathophysiology of psoriatic arthritis?

A

An environmental trigger, probably infectious in nature, triggers the disease in genetically susceptible individuals, leading to immune activation involving dendritic cells and T cells.
CD8+T cells (which recognise antigen presented in the context of HLA class I) are more abundant than CD4+T cells within the joint, which is in keeping with the genetic association between PsA and HLA-B and HLA-C variants.
There is increasing evidence that the IL-23/IL-17 pathway plays a pivotal role in PsA.
It is thought the trgigering stimulus causes over-production of IL-23 by dendritic cells, which in turn promotes differentiation and activation of Th17 cells, which produce the pro-inflammatory cytokine IL-17A.
This, along with Th1 cytokines like IFN-gamma and TNF-alpha, acts on macrophages and tissue resident stromal cells at the entheses, in bone and within the joint to produce additional pro-inflammatory cytokines and other mediators, which contribute to inflammation and tissue damage.

46
Q

What are the clinical features of psoriatic arthritis?

A

Presentation is with pain and stiffness affecting joints, tendons, spine and entheses.
Joints are typically not swollen; however, several patterns of joint involvement are recognized. - these patterns are not mutually exclusive.
Marked variation in disease pattern exists, including a disease course of intermittent exacerbation and remission.
Destructive arthritis and disability are uncommon, except in the case of arhritis mutilans.

47
Q

What are the typical patterns of joint involvement in psoriatic arthritis?

A

Asymmetrical inflammatory mono/oligo-arthritis
Symmetrical polyarthritis
Distal interphalangeal joint arthritis
Psoriatic spondylitis
Arthritis mutilans
Enthesitis-predominant

48
Q

What is Asymmetrical inflammatory mono/ oligo arthritis pattern of joint pain in PsA?

A

Often presents abruptly with combination of synovitis and adjacent periarticular inflammation.
Occurs most characteristically in the hands and feet, when synovitis of a finger or toe is coupled with tenosynovitis, enthestis and inflammation of intervening tissue to give a sausage digit or dactylitis.
Large joint like the knee and ankle, may also be involved, sometimes with very large effusions.

49
Q

What is Symmetrical polyarthritis pattern of joint pain in PsA?

A

Accounts for about 25% of cases
Predominates in women and may resemble RA, with symmetrical involvement of small and large joints in both upper and lower limbs.
Nodules and other extra-articular features of RA are absent, and arthritis is generally less extensive and more benign.

50
Q

What is tenosynovitis?

A

Tenosynovitis is the inflammation of the fluid-filled sheath (called the synovium) that surrounds a tendon, typically leading to joint pain, swelling, and stiffness.

51
Q

What is distal interphalangeal joint arthritis pattern of joint pain in PsA?

A

Can be difficult to distinguish from inflammatory generalised OA.
PsA DIP joint disease is associated with psoriatic nail disease.

52
Q

What is psoriatic spondylitis pattern of joint pain in PsA?

A

This type presents with inflammatory back or neck pain and prominent stiffness symptoms.
Any structure in the spine can be involved, including intervertebral disc entheses and facet joints.
It may occur alone or with any of the other clinical patterns described above and is typically unilateral or asymmetric in severity.

53
Q

What is arthritis mutilans pattern of joint pain in PsA?

A

Deforming erosive arthritis targeting the fingers and toes.
Occurs in 5% of PsA cases
Prominent cartilage and bone destruction results in marked instability.
The encasing skin appears invaginated and ‘telescoped’ and the finger can be pulled back to its original length.

54
Q

What is the enthesitis-predominant pattern of joint pain in PsA?

A

Presents with pain and stiffness at the insertion sites of tendons and ligaments into bone (enthesitis).
Symptoms can be extensive or localised
Nail chnages include pitting, onycholysis, subungual hyperkeratosis and horizontal ridging, which are foud in 85% of patients with PsA and can occur in the absence of skin disease.
Characteristic rash of psoriasis may be widespread or confined to the scalp, natal cleft, umbilicus and genitals, where it is easily overlooked.
Obtaining a history of psoriasis in a first degree relative can be tricky but is important, given a positve response contributes to making a diagnosis.

55
Q

What investigations should be performed to confirm a diagnosis of PsA?

A

Diagnosis is made on clinical grounds:
Autoantibodies generally negative and ESR and CRP are raised in a proportion of patients with active disease.
X-rays may be normal or show erosive change with joint space narrowing.
MRI and ultrasound with power Doppler are increasingly employed to detect synovial inflammation and inflammation at the entheses.

56
Q

What is the management of PsA?

A
  • therapy with NSAIDs and analgesics may be sufficient to manage symptoms in mild disease.
  • Intra-articular glucocorticoid injections can control isolated synovitis or enthesitis.
  • Splints and prolonged rest should be avoided because of the tendency to fibrous and bony ankylosis.
  • Patients with spondylitis should be prescribed the same exercise and posture regime as in axSpA and AS.
  • Therapy with DMARDs should be considered for persistent synovitis unresponsive to conservative treatment.
  • Methotrexate is the drug of first choice and is also effective for skin disease.
  • Other DMARDs may also be helpful, including sulfasalazine, ciclosporin and leflunomide
  • Hydroxychloroquinine generally avoided.
  • Anti-TNF treatment should be considered for individuals with active synovitis who respond inadequately to standard DMARDs
  • Ustekinumab improves joint dacytlitis, and enthesitis lesions in PsA.
  • Secukinumab has similar efficacy to TNF therapy
  • Apremilast is effective in PsA when DMARD therapy fails
57
Q

What percent of IBD patients have involvement of peripheral joints?

A

20%

58
Q

What percentage of IBD patients have radiographic evidence of sacriolitis present?

A

20-25%

59
Q

How does arthritis present in crohn’s disease?

A

Arthritis usually coincides with exacerbations of the underlying bowel disease and the arthritis improves with effective treatment of the bowel disease.

60
Q

What medication should be used in enteropathic spondyloarthritis?

A

NSAIDs are best avoided, as they can exacerbate IBD.
Judicious used of glucocorticoids, sulfasalazine and methotrexate may be considered.
Anti-TNF therapy is effective in enteropathic arthritis but etanercept should be avoided, as it has no efficacy in IBD.

Rheumatology (2 decks)

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