Inflammatory Autoimmune Seronegative Arthritis Flashcards

Psoriatic Arthritis Reactive Arthritis Ankylosing Spondylitis

1
Q

Outline the epidemiology of psoriatic arthritis.

A
  • Psoriatic arthritis occurs equally in men and women, although earlier disease onset is observed in males
  • The incidence of psoriatic arthritis in women peaks in the 6th decade, mirroring an age-specific rise in the incidence of the skin disease in females
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2
Q

What are the risk factors of psoriatic arthritis (2)?

A
  • Psoriasis
  • FHx of psoriasis or psoriatic arthritis
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3
Q

Outline the pathogenesis of psoriatic arthritis.

A

The aetiology of psoriatic arthritis is largely unknown
* Trauma to joints or tendons has been implicated in triggering psoriatic arthritis, as have infections (particularly HIV infection). Infection possibly triggers psoriatic arthritis by exposing antigens to the innate immune system and leading to expression of the psoriatic phenotype.

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4
Q

Outline the pathophysiology of psoriatic arthritis.

A

Dominant pathogenic pathway is interleukin 17/ interleukin 23

  1. Psoriatic arthritis is a disease of the cellular immune system, with CD8+ T cells playing a primary role in both the skin and synovium
  2. Compared with rheumatoid synovium, psoriatic synovium is characterised by hypervascularity and morphologically tortuous vessels
  3. Cytokine interaction with the receptor activator of nuclear factor kappa B (RANKL) leads to osteoclast proliferation and activation, contributing to erosions and osteolysis
  4. This is manifested clinically by the radiological changes of arthritis mutilans, including pencil-in-cup deformities, as well as new-bone formation of periostitis

The presence of distal interphalangeal (DIP) joint involvement and dactylitis uniquely distinguishes psoriatic arthritis from rheumatoid arthritis. These manifestations are related, respectively, to extensor tendon enthesitis at the nail bed and flexor tenosynovitis of the entire digit

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5
Q

How would a patient with psoriatic arthritis presented (5)?

A
  • Personal or Fx of psoriasis
  • Joint pain and stiffness
    • Inflammatory joint pain is characterised by prolonged morning stiffness (>30 minutes), improvement with use, and recurrence with prolonged rest.
  • Peripheral arthritis
    • Usually indicated by swelling and tenderness of individual joints (synovitis) during inspection and palpation.
    • Psoriatic arthritis frequently presents in a pattern of monoarticular or oligoarticular joint involvement. In patients with multiple joints involved, the pattern lacks the symmetry of rheumatoid arthritis.
  • Dactylitis (sausage finger) due to enthesitis
  • Hx of scalp or nail problems
    • Patients may not know they have psoriasis. The disease may be misinterpreted as scalp dandruff, seborrhoea, or onychomycosis.
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6
Q

What investigations are suggested in suspected psoriatic arthritis (8)?

A
  • Plain film X-rays of the hands and feet
  • Erythrocyte sedimentation rate and C-reactive protein (ESR & CRP)
  • Rheumatoid factor (RF)
  • anticyclic citrullinated peptide (Anti-CCP) antibody
  • Lipid profile
  • Fasting blood glucose
  • Uric acid level
  • Synovial fluid aspiration and analysis
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7
Q

What would an X-Ray show in a patient with psoriatic arthritis?

A
  • Erosion in the distal interphalangeal (DIP) joint and periarticular new-bone formation
  • Osteolysis and pencil-in-cup deformity in advanced disease
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8
Q

What would an erythrocyte sedimentation rate and C-reactive protein (ESR & CRP) test show in a patient with psoriatic arthritis?

A
  • Normal or elevated
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9
Q

What would a rheumatoid factor (RF) test show in a patient with psoriatic arthritis?

A
  • Positive or negative
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10
Q

What would an anticyclic citrullinated peptide (Anti-CCP) antibody test show in a patient with psoriatic arthritis?

A
  • Negative
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11
Q

What would a lipid profile test show in a patient with psoriatic arthritis?

A
  • Normal or hyperlipidaemia
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12
Q

What would a fasting blood glucose test show in a patient with psoriatic arthritis?

A
  • Normal or hyperglycaemia
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13
Q

What would a uric acid level test show in a patient with psoriatic arthritis?

A
  • Normal or elevated
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14
Q

What would a synovial fluid aspiration and analysis show in a patient with psoriatic arthritis?

A
  • Absence of monosodium urate crystals
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15
Q

What is the treatment of acute psoriatic arthritis (1st line 1 / Consider 2)?

A

1st line:
* Non-steroidal anti-inflammatory drugs (NSAIDs)

Consider:
* Physiotherapy
* Intra-articular corticosteroid injection

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16
Q

Outline the epidemiology of reactive arthritis.

A
  • Unclear
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17
Q

What are the risk factors of reactive arthritis (3)?

A
  • Male sex
  • HLA-B27 genotype
  • Preceding chlamydial or gastrointestinal infection
18
Q

Outline the pathogenesis of reactive arthritis.

A
  • The bacteria associated with ReA are common causes of venereal disease and infectious dysentery
    • They are gram-negative organisms, with a lipopolysaccharide component within their cell wall

The most commonly implicated bacterial species are Chlamydia, Salmonella, Campylobacter, Shigella, and Yersinia species, although ReA has been described after many other bacterial infections

19
Q

Outline the pathophysiology of reactive arthritis.

A
  • Unclear mechanism, however bacterial DNA of known infectious triggers has been discovered in the synovial tissue of patients with ReA.

Sterile inflammation in joints following infection elsewhere in the body
* Reactive arthritis NOT the same as infection in joints (septic arthritis)

20
Q

How would a patient with reactive arthritis present (6)?

A
  • Presence of risk factors
  • Peripheral arthritis
    • Assymetrical oligoarthritis within 1 to 4 weeks after the onset of infection
  • Axial arthritis (Axial inflammation)
  • Constitutional symptoms
    • Fever, fatigue, and weight loss are common
  • Enthesitis (inflammation at sites where tendons insert into bones)
  • Skin and eye inflammation
Keratoderma blenorrhagia in a patient with reactive arthritis
21
Q

What investigations are suggested in suspected reactive arthritis (7)?

A
  • Erythrocyte sedimentation rate (ESR)
  • C-reactive protein (CRP)
  • Antinuclear antibody (ANA)
  • Rheumatoid factor (RF)
  • Urogenital and stool cultures
  • Plain X-rays
  • Arthrocentesis with synovial fluid analysis
22
Q

What would an erythrocyte sedimentation rate (ESR) test show in a patient with reactive arthritis?

A
  • Elevated
23
Q

What would a C-reactive protein (CRP) test show in a patient with reactive arthritis?

A
  • Elevated
24
Q

What would an antinuclear antibody (ANA) test show in a patient with reactive arthritis?

A
  • Negative
25
Q

What would a rheumatoid factor (RF) test show in a patient with reactive arthritis?

A
  • Negative
26
Q

What would a urogenital and stool cultures test show in a patient with reactive arthritis?

A
  • Negative unless patients are tested very early after onset of infection
27
Q

What would a plain X-Ray show in a patient with reactive arthritis?

A

Sacroiliitis or Enthesopathy

Sacroiliitis

Sacroiliitis is an inflammation of the sacroiliac joint (SI), usually resulting in pain.

Entheses are boney insertion sites of tendons and ligaments. Enthesopathies are defined as the pathologies that affect the entheses.

28
Q

What would an arthrocentesis with synovial fluid analysis show in a patient with reactive arthritis?

A
  • Negative
29
Q

What is the treatment for acute reactive arthritis (1st line 1 / consider 1)?

A

1st line:
* Non-steroidal anti-inflammatory drug (NSAID)

Consider:
* Corticosteroid

30
Q

What is the treatment for ongoing reactive arthritis (1st line 1)?

A

1st line:
* Disease-modifying antirheumatic drug (DMARD)

31
Q

Outline the epidemiology of ankylosing spondylitis (AS).

A
  • HLA-B27 is present in about 90% of patients who have AS
32
Q

What are the risk factors of ankylosing spondylitis (AS) (4)?

A
  • HLA-B27
  • Endoplasmic reticulum aminopeptidase 1 (ERAP1) and interleukin-23 receptor (IL23R) genes
  • Positive Fx of AS
  • Male sex
33
Q

Outline the pathogenesis of ankylosing spondylitis (AS).

A

HLA-B27 is present in about 90% of patients who have AS. HLA-B27 contribution to the total genetic risk for AS is, however, relatively modest (approximately 20%).
* The role of HLA-B27 in the pathogenesis of AS remains largely unclear.

34
Q

Outline the pathophysiology of ankylosing spondylitis (AS).

A
  • largely genetic component (polygenic)
  • HLA-B27 is the strongest genetic risk factor (class 1 MHC molecule associated with CD8 T cells
  • cytokines- TNF- alpha, IL17, IL23
  • abherrant peptide processing pathways (aminopeptidases in the endoplasmic reticulum)
35
Q

How would a patient with ankylosing spondylitis (AS) present (4)?

A
  • Presence of risk factors
  • Inflammatory back pain
  • Iritis / Uveitis
  • Enthesitis
  • Apical lung fibrosis, aortitis, amyloidosis
36
Q

What investigations are suggested in suspected ankylosing spondylitis (AS) (1)?

A
  • Pelvic X-Ray
37
Q

What would a pelvic X-Ray show in a patient with ankylosing spondylitis (AS)?

A

Sacroiliitis

38
Q

What is the treatment for acute ankylosing spondylitis with pain and / or stiffness (1st line 1 / consider 1)?

A

1st line:
* Non-steroidal anti-inflammatory drug (NSAID) + non-pharmacological therapy

Consider:
* Analgesic

39
Q

What is the treatment for acute ankylosing spondylitis without pain and / or stiffness (1st line 1)?

A

1st line:
* Re-assessment and observation

40
Q

What is the treatment for ongoing ankylosing spondylitis with pain and / or stiffness (1st line 2 / consider 1)?

A

1st line:
* Tumour necrosis factor (TNF)-alpha inhibitor
* Physiotherapy

Consider:
* continued non-steroidal anti-inflammatory drug (NSAID)