Osteoarthritis and reactive arthritis Flashcards

(36 cards)

1
Q

What is reactive arthritis?

A

It is a reaction to an infectious trigger (not current infection). Sterile inflammation in joints following infection, especially urogenital (e.g. Chlamydia trachomatis) and gastrointestinal (e.g. Salmonella, Shigella, Campylobacter infections) infections

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2
Q

What is septic arthritis?

A

If there is an infection in a joint at present

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3
Q

What is affected in reactive arthritis?

A

Joints and extra-articular areas

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4
Q

What are some extra-articular manifestations of reactive arthritis?

A
  • Enthesopathy (overlap between reactive arthritis and seronegative spondyloarthropathies)
  • Skin inflammation
  • Eye inflammation
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5
Q

What may reactive arthritis be a manifestation of?

A

Hep C

HIV

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6
Q

Who is affected by reactive arthritis?

A

Young adults with a genetic predisposition and an environmental trigger. Could be an infection and symptoms follow 1-4 weeks after the infection

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7
Q

What is the HLA associated with reactive arthritis?

A
HLA- B27
MHC class 1
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8
Q

What are the symptoms of reactive arthritis?

A

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

ENTHESITIS: there are manifestations involving inflammation of the enthesis:

  • 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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9
Q

What are the differences between rheumatoid arthritis and reactive arthritis?

A
  • Reactive arthritis, the pattern is asymmetrical but in rheumatoid it is symmetrical
  • In rheumatoid, the atlanto-axial joint can be involved, however, there is no thoracic and lumbar involvement (not synovial joints)
  • Rheumatoid affects more than 5 joints but reactive is less than 5
  • In reactive arthritis, just like in ankylosing spondylitis, this phenomenon can occur
  • RF in RA
  • Larger joints in reactive but RA can be in small and large
  • Different HLAs
  • All ages in RA and reactive is young (20-40)
  • Reactive more common in males whilst rheumatoid is females
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10
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 fee

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11
Q

How is reactive arthritis diagnosed?

A

To diagnose exclude other causes of arthritis e.g. septic

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 because 9% of the population are positive)

Synovial fluid examination:
- Especially if only single joint affected

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12
Q

Compare septic arthritis and reactive arthritis

A
  • Reactive the fluid is sterile but in septic it is infected
  • In septic antibiotics are needed
  • In septic joint lavage may be needed for large joints but not in reactive
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13
Q

Does reactive arthritis resolve?

A

In the majority of patients, complete resolution occurs within 2-6 months. There is no role for antibiotics. In the mean time, we want to reduce inflammation and control pain.

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14
Q

How are is reactive arthritis treated?

Articular and extra-articular

A

Articular: NSAIDs, intra-articular corticosteroid therapy

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

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15
Q

How is refractory disease treated (reactive arthritis)?

A
  • Oral glucocorticoids

- Steroid-sparing agents e.g. sulphasalazine

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16
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), spine and weight-bearing joints (hips and knees)

17
Q

What is affected in osteoarthritis?

A

Joints of the hand

  • Distal interphalangeal joints (DIP)
  • Proximal interphalangeal joints (PIP)
  • First carpometacarpal joint (CMC)

Spine

Weight-bearing joints of lower limbs

  • Especially the knees and hips
  • First metatarsophalangeal joint (MTP)
18
Q

What are the signs of osteoarthritis in the hands?

A

Heberden’s nodes and Bouchard’s nodes are simply referring to bony outgrowths at particular joints.

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

OUCHARD’S NODES: bony swellings around the proximal interphalangeal joints.

19
Q

What is associated with osteoarthritis?

A
  • Joint pain: worse with activity, better with rest
  • 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
20
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
21
Q

What are the differences in the radiographic changes in rheumatoid and osteoarthritis?

A
  • In RA: joint space narrowing, no subchondral sclerosis, no osteophytes, osteopenia and bony erosions
  • In osteoarthritis, joint space narrowing, subchondral sclerosis, osteophytes, no osteopenia (weak bones) and no bony erosions
  • Juxta-articular osteopenia is common early radiographic sign in inflammatory arthritis of any cause.
  • Erosions occur initially at the margins of the joint where the synovium is in direct contact with bone (the ‘bare’ area)
22
Q

What happens to cartilage and bone in osteoarthritis?

A

In osteoarthritis, there is defective and irreversible articular cartilage and damage to underlying bone

23
Q

What can cause osteoarthritis?

A
  • Excessive loading on the joints
  • Abnormal joint components
  • Aging, metabolic causes, endocrine factors etc.
24
Q

Describe the structure and makeup of the articular cartilage

A
  • Weight-bearing properties of articular cartilage depend on intact collagen scaffold and high aggrecan content
  • Articular cartilage is avascular, and is an aneural structure
  • Collagen type II
  • There are large, proteoglycan monomers: main one is aggrecan, its huge
  • The aggrecan contains glycosaminoglycan side chains (e.g. chondroitin sulphate, keratin sulphate)
  • The negative charge of the GAG attracts water, keeping the cartilage hydrated
  • When this is lost, articular cartilage becomes fragile and begins to break down
25
What causes cartilage to become fragile?
- The negative charge of the GAG attracts water, keeping the cartilage hydrated - When this is lost, articular cartilage becomes fragile and begins to break down
26
What are GAGs? Give examples What are proteoglycans? Give examples
Proteoglycans: glycoproteins containing one or more sulphated glycosaminoglycan (GAG) chains: - Intracellular: serglycin - Cell surface associated: betaglycan, syndecan - Secreted into ECM: aggrecan, decorin, fibromodulin, lumican, biglycan GAGs are repeating polymers of disaccharides and include: - Chondroitin sulphate - Heparan sulphate - Keratan sulphate - Dermatan sulphate - Heparin
27
What is the major proteoglycan in articular cartilage? What is a major component of synovial fluid?
- Aggrecan - Hyaluronic acid is the only non-sulphated GAG and is major component of synovial fluid (important role in maintaining synovial fluid viscosity)
28
What are the disaccharides of hyaluronic acid?
glucuronic acid and N-acetyl glucosamine
29
What are the cartilage changes in osteoarthritis?
- Reduced proteoglycan - Reduced collagen - Chondrocyte changes e.g. apoptosis - Localised changes
30
What are the bone changes in osteoarthritis?
- Changes in exposed 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 - Osteophytes
31
How is osteoarthritis managed?
- 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
32
What are some therapeutic approaches for osteoarthritis not recommended by NICE?
- Glucosamine and chondroitin sulphate – commonly taken | - Intra-articular injections of hyaluronic acid
33
Glucosamine and chondroitin sulphate - how are they raken and why is it not recommended by NICE?
- Dietary supplementation commonly taken by patients - Some studies suggesting improvement in pain (may be a placebo effect) - No clear evidence that oral intake alters articular cartilage composition
34
Intra-articular injections of hyaluronic acid - what does it do, where is it used experimentally?
- 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
35
What are some future therapies for osteoarthritis?
Stop matrix breakdown, aggrecanase inhibitors, cytokine inhibitors, stimulate repair of matrix
36
What is enthesis?
The connective tissue between tendon or ligament and bone