Rheum - Reactive Arthritis Flashcards

1
Q

Define Reactive Arthritis

A

STERILE inflammation in joints FOLLOWING infection especially
• urogenital (e.g. Chlamydia) & gastrointestinal (e.g. Salmonella, Shigella) infections

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2
Q

Key points associated with Reactive Arthritis?

A

Important extra-articular manifestations include:
• Enthesopathy – a disorder relating to the ligament attaching to the bone
• Skin inflammation
• Eye inflammation

ReA may be the first manifestation of HIV or Hep C infection

Commonly affects young adults (with a genetic disposition – e.g. HLA-B27) with an environmental trigger such as a Salmonella infection

Symptoms follow 1-4 weeks after infection (may be mild)

ReA is distinct (sterile) from infection in the joints
• known as SEPTIC arthritis.

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3
Q

Is there a biomedical test to check for ReA?

A

NO as it is ‘seronegative’

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4
Q

Musculoskeletal symptoms of ReA?

A

Arthritis:
 Asymmetrical
 Oligoarthritis – less than 5 joints affected
 Lower limbs more affected

Enthesitis:
 Heel pain – Achilles tendonitis
 Swollen fingers – dactylitis
 Painful feet – metatarsalgia due to plantar fasciitis

Spondylitis:
 Sacroiliitis – inflammation of the sacro-iliac joint
 Spondylitis – inflammation of the spine

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5
Q

Extra-articular features of ReA?

A

Ocular:
 Sterile conjunctivitis

Genito-urinary:
 Sterile urethritis

Skin:
 Circinate balanitis
 Keratoderma blennorrhagicum

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6
Q

What was the original description of ReA?

A

arthritis, urethritis and conjunctivitis following infectious dysentery (Reiter’s syndrome)

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7
Q

Compare RA vs. ReA

A

Onenote!!

Sex Ratio
Age
Arthritis
Enthesopathy
Spondylitis
Urethritis
Skin involvement
Rheumatoid factor
HLA association
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8
Q

Compare Spetic A vs. ReA?

A

Onenote!!

Synovial fluid culture
Antibiotic therapy
Joint Lavage

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9
Q

What is one of the biggest things about RA in the comparison table

A

Note how RA affects the ATLANTO-AXIAL JOINT (

• as this spinal joint contains synovial fluid

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10
Q

How is diagnosis achieved for ReA?

A

3 main ways:

Clinical diagnosis – i.e. asymmetrical arthritis

Investigations of exclusion – i.e. septic arthritis

Other investigations:
• Microbiology:
- Microbial cultures – stool, blood, etc.
- Serology – e.g. HIV, Hep C.

• Immunology:

  • RF.
  • HLA-B27.

• Synovial fluid examination – only if a single joint is affected.

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11
Q

How is ReA treated?

A

In majority, resolution in 2-6months

NO ROLE for antibiotics

Articular:
• NSAIDs
• Intra-articular corticosteroid therapy

Extra-articular:
• Symptomatic therapy – topical steroids

Refractory disease – non-responsive to treatment:
• Oral glucocorticoids
• Steroid-sparing agents – DMARDs

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12
Q

Define Osteoarthritis

A
Chronic, slowly progressive disorder due to failure of articular cartilage, typically affecting joints of the
 • hand
 • spine 
and 
 • weight-bearing joints
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13
Q

What joints does osteoarthritis normally affect?

A

Joints of the hand
• DIP, PIP, CMC (1st carpometacarpal joint)
• NOT MCP
- Herberden’s nodes - osteophytes at DIP joints
- Bouchard’s nodes – osteophytes at PIP joints
Before (proximal) = Bouchard

Spine

Weight-bearing joints of the lower limbs
• hip/knee, MTP (1st metatarsophalangeal joint)

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14
Q

What is osteoarthritis associated with?

A

o Joint pain
• worse with activity

o Joint crepitus
• creaking sound on movement

o Joint instability

o Joint enlargement
• i.e. Herberden’s nodes.

o Joint stiffness after immobility and limitation of motion.

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15
Q

What are radiographic features of osteoarthritis?

A

o Joint space narrowing

o Subchondral bony sclerosis
• hardening of the bone on the subchondral portion

o Osteophytes
• new bony formations (at joint margins)

o Subchondral cysts

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16
Q

Radiographic changes in RA vs. OA?

A

Onenote!!

Joint space narrowing
• occurs in BOTH due to different reasons
• cartilaginous loss in RA is caused by 2o damage due to synovitis vs. in OA where is it the 1o abnormality

Subchondral sclerosis
Osteophytes
Osteopenia
Bony erosions

17
Q

Pathogenesis of OA?

A

There is defective and irreversible articular cartilage and damage to the underlying bone

This develops due to (and/or):
• Excessive loading on joints – more apparent in the old
• Abnormal joint components – more apparent in the young

18
Q

What is the most important component of the articular cartilage?

A

AGGRECAN!

The weight-bearing properties of the articular cartilage depend upon the
• intact collagen scaffold & the high aggrecan content

Aggrecan is made up of
• Chondroitin sulphate & Keratan sulphate
• The GAG chains are important at absorbing water to be used to resist compressive forces.

19
Q

Explain ECM proteoglycans

A

Proteoglycan – glycoproteins containing 1+ sulphated glycosaminoglycans (GAG) chains

GAGs are repeating polymers of disaccharides and include:
	Chondroitin sulphate.
	Heparan sulphate.
	Keratan sulphate.		
	Dermatan sulphate.		
	Heparin.

Examples:
 Intra-cellular – Serglycin.
 Cell-surface associated – Betaglycan, Syndecan.
 Secreted into ECM – Aggrecan, Decorin, Fibromodulin, Lumican, Biglycan.

20
Q

What in unique about Hyaluronic acid?

A

Is the ONLY non-sulphated GAG

• and has an important role in maintaining synovial fluid viscosity

21
Q

What is the major proteoglycan in articular cartilage?

A

Aggrecan

22
Q

Explain the cartilage changes in OA

A

Reduced proteoglycan
Reduced collagen
Chondrocyte changes
• e.g. apoptosis

23
Q

Explain the bone changes in OA

A

Changes in sub-articular bone:
• Proliferation of superficial osteoblasts resulting in sclerotic bone
• Focal stress on sclerotic bone  focal superficial necrosis

New bone formation at joint margins (bone spurs):
• Examination can detect these.
• Herberden’s nodes vs Bouchard’s nodes.

24
Q

Management of OA?

A

o Education.
o Physical therapy.
o Occupational therapy.
o Weight loss (where appropriate) and exercise.
o Analgesia – paracetamol, NSAIDs, intra-articular corticosteroid injections.
o Joint replacements.

Provided the joint is functional, all you have to do is CONTROL the PAIN
• strengthening the muscle around the joint will improve mechanical stability of the joint

25
Q

What are some therapeutic approached for OA, NOT approved in UK?

A

Glucosamine and chondroitin sulphate supplements
• commonly taken but not approved by NICE

Intra-articular injections of hyaluronic acid
• to increase lubrication in the knee only
• not recommended by NICE

Unlike RA, no DMOADs (Disease-Modifying Osteoarthritis Drugs)
• Future drugs could include – aggrecanase inhibitors, cytokine inhibitors, etc.