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LCRS Musculoskeletal > Reactive Arthritis & Osteoarthritis > Flashcards

Reactive Arthritis & Osteoarthritis Flashcards

1
Q

what is reactive arthritis (ReA)?

what are the 2 types of the cause?

A

STERILE inflammation in large joints typically following infection

  • urogenital i.e. STI (e.g. Chlamydia)
  • gastrointestinal (e.g. Salmonella, Shigella)

these are gram -ve bacteria produce endotoxin LPS

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2
Q

what are the 3 important EXTRA ARTICULAR manifestations of ReA? i.e. apart from joints

A
  • Skin inflammation (Circinate balanitis; Keratoderma blennorrhagicum)
  • Eye inflammation (sterile conjunctivitis)
  • sterile urethritis (urethra infection)

Joints+Urethra+Conjunctiva= Reiter Syndrome

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3
Q

what infections might ReA be the first manifestation of?

A

HIV

Hep C infections

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4
Q

who does ReA mostly affect?

A 
young adults (20-40) 
more common in males
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5
Q

what is a genetic component in ReA?

A

e.g. HLA-B27

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6
Q

what is an environmental component in ReA?

A

e.g. Salmonella infection

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7
Q

how is ReA different to infection in the joints?

A

ReA is sterile while infection in the joints is septic arthritis

septic arthritis tends to be mono-arthritic most times

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8
Q

why is there no biochemical test to check for ReA?

A

there is no rheumatoid factor i.e. ReA is seronegative

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9
Q

what are the 3 categories of musculoskeletal symptoms in ReA?

A

o Arthritis
o Enthesitis
o Spondylitis

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10
Q

what are the arthritic symptoms of ReA?

A

 Asymmetrical.
 Oligoarthritis – less than 5 joints affected.
 Lower libs more affected.

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11
Q

what are the enthesitic symptoms of ReA?

A

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

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12
Q

what are the spondylitic symptoms of ReA?

A

 Sacroiliitis – inflammation of the sacro-iliac joint.

 Spondylitis – inflammation of the spine.

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13
Q

what are the extras-articular features of ReA?

A

o Ocular:
- Sterile conjunctivitis.

o Genito-urinary:
- Sterile urethritis.

o Skin:

  • Circinate balanitis.
  • Keratoderma blennorrhagicum

[from the original description of ReA: arthritis, urethritis and conjunctivitis following infectious dysentery (Reiter’s syndrome)]

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14
Q

how does arthritis compare in RA and ReA?

A

RA:
- Symmetrical; polyarticular; small and large joints affected

ReA:
- asymmetrical; oligoarticualr; large joints

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15
Q

how does skin involvement differ in RA and ReA?

A

RA:
- subcutaneous nodules

ReA:

  • Circinate balanitis.
  • Keratoderma blennorrhagicum
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16
Q

what is the HLA association in RA and in ReA?

A

RA: HLA-DR4

ReA: HLA-B27

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17
Q

how does the synovial fluid culture compare in septic arthritis and ReA?

A

SA: positive
ReA: sterile

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18
Q

which of SA and ReA required antibiotic therapy?

A

SA

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19
Q

which of SA and ReA requires a joint lavage?

A

SA

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20
Q

why does RA affect the Atlanto-axial joint despite not causing widespread spondylitis?

A

this joint contains synovial fluid

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21
Q

what are the main methods of diagnosing ReA?

  • clinical diagnosis i.e. feature?
  • exclusion of?
  • other investigations?
A

Clinical diagnosis – i.e. asymmetrical arthritis.

Investigations of exclusion – i.e. septic arthritis

Other investigations:
- Microbiology: 
    cultures – stool, blood, etc.
    serology – e.g. HIV, Hep C.
- Immunology: RF, HLA-B27.
- Synovial fluid examination – only if a single joint is affected.
22
Q

what is the treatment for the articular features of ReA?

A

o NSAIDs.

o Intra-articular corticosteroid therapy.

23
Q

what is the treatment or the extra-articular features of ReA?

A

o Symptomatic therapy – topical steroids

24
Q

what is the treatment for refractory ReA?

A

when non-responosve to treatment:
o Oral glucocorticoids.
o Steroid-sparing agents – DMARDs.

25
Q

what is osteoarthritis?

A

chronic, slowly progressive disorder due to failure of articular cartilage, typically affecting joints of the hand, spine and weight-bearing joints.

26
Q

what joints of the hand are affected by OA?

A

DIP
PIP
CMC (1st carpometacarpal joint)

not the MCPs

27
Q

what nodes are found in the hands as a result of OA? which joints are they found in?

A

 Herberden’s nodes - osteophytes at DIP joints.

 Bouchard’s nodes – osteophytes at PIP joints. (comes Before)

28
Q

what are the weight-bearing joints affected by OA?

A

hip/knee

MTP (1st metatarsophalangeal joint).

29
Q

what is OA symptomatically associated with in the joints?

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.

30
Q

what are the main radiographic features in OA?

A 
o	Joint space narrowing
o	Subchondral bony sclerosis 
– hardening of the bone on the subchondral portion.
o	Osteophytes 
– new bony formations.
o	Subchondral cysts.
31
Q

which radiographic features define OA?

A

subchondral sclerosis
osteophytes are strongly associated with OA

osteopenia and bony erosions would indicate RA

joint space narrowing occurring in both OA and RA for different reasons

32
Q

what is the pathogenesis of OA?

A

defective and irreversible articular cartilage and damage to the underlying bone due to:
 Excessive loading on joints – more apparent in the old.
 Abnormal joint components – more apparent in the young.

33
Q

in which group of people are abnormal joint components contributing to OA?

A

in the young

34
Q

what is important for the weight-bearing properties of the articular cartliage?

A

the intact collagen scaffold and high aggrecan content

35
Q

what is aggrecan made of?

A

Chondroitin sulphate and Keratan sulphate

GAG chains

36
Q

what is the significance of GAG chains in aggrecan?

A

absorbing water to resist compressive forces

37
Q

what type of molecule are proteoglycans?

A

glycoproteins containing 1+ sulphated glycosaminoglycans (GAG) chains

38
Q

what are the different GAGs?

A 
	Chondroitin sulphate.
	Heparan sulphate.
	Keratan sulphate.		
	Dermatan sulphate.		
	Heparin.

hyaluronic acid only non-sulphated GAG

39
Q

what is the major proteoglycan in articular cartliage?

40
Q

what is the role of hyaluronic acid?

A

is the only non-sulphated GAG and has an important role in maintaining synovial fluid viscosity

41
Q

example of proteoglycans and their locations

A

Intra-cellular
– Serglycin.

 Cell-surface associated – Betaglycan, Syndecan.

Secreted into ECM
– Aggrecan, Decorin, Fibromodulin, Lumican, Biglycan.

42
Q

what are the cartilage changes in OA?

A

 Reduced proteoglycan.
 Reduced collagen.
 Chondrocyte changes
– e.g. apoptosis.

43
Q

what leads to sclerotic changes in bone?

A

proliferation of superficial osteoblasts

44
Q

what leads to focal superficial necrosis?

A

focal stress on sclerotic bone

45
Q

what are the sub-articular changed in bone in OA?

A
  • sclerotic bone

- focal superficial bone

46
Q

what are bone spurs?

A

new bone formations at joint margins

47
Q

what are the management options 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.

48
Q

what are some therapeutic options (not approved in the UK)?

A

o Glucosamine and chondroitin sulphate supplements (taken but not approved by NICE)

o Intra-articular injections of hyaluronic acid – to increase lubrication in the knee only (not approved by NICE)

there are no Disease-Modifying Osteoarthritis Drugs

49
Q

what are potential future drugs?

A

aggrecanase inhibitors, cytokine inhibitors

50
Q

why is denosumab (RANKL analogue) used to treat osteoporosis?

A

RANKL (produced by osteoblasts) causes osteoclast activity (by binding to their RANK receptors) and therefore bone resorption

TNFalpha increases RANKL and therefore worsens osteoporosis

51
Q

what is Enthesopathy?

A

disorder related to the ligament attaching to the bone

LCRS Musculoskeletal (11 decks)

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