Osteoarthritis and Reactive Arthritis Flashcards

1
Q

What is reactive arthritis?

A

sterile inflammation in joints following infection, especially urogenital (e.g. Chlamydia trachomatis) and gastrointestinal (e.g. Salmonella, Shigella, Campylobacter infections) infections

may be the first manifestation of HIV or hepatitis C infection

commonly affects young adults with genetic predisposition and environmental trigger e.g genetic predisposition could be HLA-B27, and environmental trigger could be salmonella infection

  • distinct from infection in joints (septic arthritis)
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2
Q

What areas are affected by reactive arthritis?

A

Joints AND extra-articular areas are affected

e. g Enthesopathy (overlap between reactive arthritis and seronegative spondyloarthropathies)
- Skin inflammation
- Eye inflammation

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3
Q

What are the musculoskeletal symptoms of reactive arthritis?

A

ARTHRITIS: asymmetrical, oligoarthritis (<5 joints), lower limbs are typically affected

ENTHESITIS:

  • Heel pain (Achilles tendonitis)
  • Swollen fingers (dactylitis)
  • Painful feet (metatarsalgia due to plantar fasciitis)

SPONDYLITIS: predilection for spinal inflammation:

  • Sacroiliitis (inflammation of the sacro-iliac joints)
  • Spondylitis (inflammation of the spine)
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4
Q

What are some differences between rheumatoid arthritis and reactive arthritis?

A

reactive:
- asymmetrical
- M>F sex ratio
- 20-40yrs
- oligoarticular
- enthesopathy, spondylitis, urethritis
- no rheumatoid factor
- HLA-B27

rheumatoid:

  • symmetrical
  • no thoracic and lumbar involvement (no synovial joints)
  • F>M
  • all ages
  • polyarticular
  • no enthesopathy, spondylitis or urethritis
  • rheumatoid factor
  • HLA-DR4
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5
Q

What are the extra-articular features of reactive arthritis?

A
  • Ocular: sterile conjunctivitis
  • Genito-urinary: sterile urethritis
  • Skin: circinate balanitis AND psoriasis-like rash on hands and feet
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6
Q

How is the diagnosis for reactive arthritis established?

A

Clinical diagnosis
- Investigations to exclude other causes of arthritis e.g. septic arthritis

Microbiological analysis:

  • Microbial cultures – blood, throat, urine, stool, urethral, cervical
  • Serology e.g. HIV, hepatitis C

Immunological tests:

  • Rheumatoid factor should be negative in reactive arthritis
  • (HLA-B27 – not particularly useful in this setting, because 9% of the population are positive)

Synovial fluid examination:
- Especially if only single joint affected

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7
Q

What are some differences between septic arthritis and reactive arthritis?

A

septic:

  • positive synovial fluid culture
  • antibiotic therapy
  • joint lavage for large joints

reactive:

  • sterile synovial fluid culture
  • no antibiotic therapy or joint lavage
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8
Q

How is reactive arthritis treated?

A
  • majority of patients, complete resolution occurs within 2-6 months. In the mean time, we want to REDUCE INFLAMMATION and CONTROL PAIN.

Articular:

  • NSAIDs
  • intra-articular corticosteroid therapy

Extra-articular:
- typically self-limiting, hence symptomatic therapy e.g topical steroids & keratolytic agents in keratoderma

Refractory disease:

  • Oral glucocorticoids
  • Steroid-sparing agents e.g. sulphasalazine
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9
Q

What is osteoarthritis?

A

Chronic slowly progressive disorder, primarily due to failure of articular cartilage that typically affecting joints of the hand (especially those involved in pinch grip - DIP, PIP, 1ST CMC), spine and weight-bearing joints (hips and knees and 1ST MTP)

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10
Q

What nodes do you get in osteoarthritis?

A

HEBERDEN’S NODES: bony, prominent swelling around the distal interphalangeal joints

BOUCHARD’S NODES: bony swellings around the proximal interphalangeal joints

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11
Q

What is osteoarthritis associated with?

A
  • Joint pain: worse with activity, better with rest (loss of articular cartilage -> mechanical failure of joints)
  • Joint crepitus: creaking, cracking, grinding sound on moving affected joint
  • Joint instability
  • Joint enlargement e.g. Heberden’s nodes
  • Joint stiffness after immobility (‘gelling’)
  • Limitation of motion
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12
Q

What are the radiographic features of osteoarthritis?

A
  • Joint space narrowing
  • Subchondral bony sclerosis (underlying bone reacting to damaged articular cartilage)
  • Osteophytes (Heberden’s and Bouchard’s nodes)
  • Subchondral cysts
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13
Q

Compare the radiographic changes in rheumatoid and osteoarthritis?

A

rheumatoid:

  • joint sparing narrowing
  • no subchondrial sclerosis
  • no osteophyles
  • osteopenia
  • bony erosions

osteoarthritis:

  • joint sparing narrowing
  • subchondrial sclerosis
  • osteophyles
  • no osteopenia
  • no bony erosions
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14
Q

What causes osteoarthritis?

A
  • Excessive loading on the joints
  • Abnormal joint components
  • very multifactorial condition. There are some rare metabolic and endocrine factors
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15
Q

Describe the structure of articular cartilage?

What causes articular cartilage to break down?

A
  • avascular and an aneural structure
  • The collagen is type II.
  • large, proteoglycan monomers. The key proteoglycan in articular cartilage is aggrecan. It is HUGE (2-3 million kDa).

The aggrecan contains glycosaminoglycan side chains (e.g. chondroitin sulphate, keratin sulphate) - negatively charged s attracts water keeping the cartilage hydrated.

When this is lost, articular cartilage becomes fragile and begins to break down.

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16
Q

What are proteoglycans?

A

glycoproteins containing one or more sulphated glycosaminoglycan (GAG) chains

17
Q

What are the different GAGs?

A
  • repeating polymers of disaccharides

include:

  • Chondroitin sulphate (disaccharides are: glucuronic acid and N-acetyl galactosamine)
  • Heparan sulphate
  • Keratan sulphate (disaccharides are: galactose and N-acetyl glucosamine)
  • Dermatan sulphate
  • Heparin
  • Hyaluronic acid is the only non-sulphated GAG and is major component of synovial fluid
18
Q

What are some examples of proteoglycans?

A
  • Intracellular: serglycin
  • Cell surface associated: betaglycan, syndecan
  • Secreted into ECM: aggrecan, decorin, fibromodulin, lumican, biglycan
19
Q

What are the cartilage changes in osteoarthritis?

A
  • Reduced proteoglycan
  • Reduced collagen
  • Chondrocyte changes e.g. apoptosis
  • CHANGES ARE OFTEN LOCALISED
20
Q

What are the bone changes in osteoarthritis (once cartilage is damaged)?

A

Changes in denuded sub-articular bone:

  • Proliferation of superficial osteoblasts results in production of sclerotic bone e.g. subchondral sclerosis
  • Focal stress on sclerotic bone can result in focal superficial necrosis
21
Q

What are osteophytes?

A

New bone formation at the joint margins

Sometimes you can detect osteophytes clinically (‘at the bedside’) and these have names

  • at the distal inter-phalangeal joints: ‘Heberden’s nodes’
  • at the proximal inter-phalangeal joints: ‘Bouchard’s nodes
22
Q

How is osteoarthritis managed?

A
  • Education
  • Physical therapy – physiotherapy, hydrotherapy (optimizing physical strength of patient)
  • Occupational therapy
  • Weight loss where appropriate
  • Exercise
  • Analgesia
    > Paracetamol
    > Non-steroidal anti-inflammatory agents
    > Intra-articular corticosteroid injection
  • Joint replacement if it comes to it – this has been a MAJOR success
23
Q

What therapeutic approaches for osteoarthritis are not approved in the UK?

A

Glucosamine and chondroitin sulphate – commonly taken

  • Dietary supplementation commonly taken by patients
  • Some studies suggesting improvement in pain (may be a placebo effect)
  • NO CLEAR EVIDENCE THAT ORAL INTAKE ALTERS ARTICUALR CARTILAGE COMPOSITION

Intra-articular injections of hyaluronic acid

  • Hyaluronic acid to increase lubrication (visco-supplementation)
  • Only used in the knee joint and still experimental
  • Not recommended by NICE but practiced a lot in private medicine