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Stage 2: Ageing > Osteoarthritis > Flashcards

Osteoarthritis Flashcards

1
Q

What is the lifetime risk of OA?

A

50%

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2
Q

What % of people age > 55 have osteoarthritis?

A

> 80% (0.1% in those aged 25-34)

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3
Q

What is osteoarthritis?

A

Damage within the cartilage of the joint which results in bone damage that surrounds that as a secondary response (much less genetic than RA)

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4
Q

OA is not just a normal consequence of ageing. What factors result in OA?

A

1) Joint integrity
2) Genetics
3) Local inflammation (inflammatory components, not primarily inflammatory disease with systemic inflammation)
4) Mechanical forces
5) Metabolic processes

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5
Q

What is the key site of the problem in OA and how is this different from RA?

A

Chondrocyte

  • In RA key site of pathology is the synovium (synovitis)
  • Osteoarthritis is a cartilage pathology (cartilage loss)
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6
Q

What is the chondrocyte?

A
  • The primary cell within cartilage although most of cartilage is ECM
  • Role = proliferation, collagen synthesis, degradation of matrix
  • Cartilage is a v slow turnover material
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7
Q

What does OA look like radiographically?

A

Cartilage loss doesn’t really show up bc it is mostly water so in OA you see loss of joint space

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8
Q

What is the link between sports and OA?

A
  • The joints affected by OA are those joints most used in that sport e.g. gymnastics = shoulders, wrists, elbows, boxing = carpometacarpals, ballet = talar joints etc
  • No link between long distance running and OA
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9
Q

What is the role of biomechanical stressors in OA?

A

1) Occupations associated with repetitive biomechanical forces e.g. carpentry linked to OA
2) Maybe linked to muscle weakness?
3) Obesity (excessive load) - associated with OA at many sites e.g. knee (8x risk), hand (3x risk) therefore not just to do with weight bearing, maybe link between cytokines produced by adipocytes which may alter cartilage turnover

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10
Q

Which gender is more at risk of OA?

A

Women (3x)

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11
Q

Describe OA in women

A
  • ‘Menopausal’ arthritis is a well-recognised phenomenon
  • Hormonal factors might play a role - oestrogen therapy may be protective (but concerns with safety)
  • There tends to be some protection from OA in childbearing years with period and then around menopause they ‘catch up’
  • They can develop what can look inflammatory initially e.g. effusions in knee joints/small joints in hands and then the OA appears with the characteristic patterns
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12
Q

Describe OA in men

A

OA symptoms in men tend to develop in 40s and gradually over many years

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13
Q

What is the relationship between OA and osteoporosis?

A

There is a negative correlation between osteoporosis (thinning of bone) and OA (overgrowth of bone)

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14
Q

What are the risk factors for OA?

A

1) Age > 40
2) Female
3) Obesity
4) Previous injury incl. biomechanical stressors (acute injury/trauma or chronic stress on joint)
5) Genetic factors

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15
Q

What is the main symptom associated with OA?

A

Pain (despite cartilage being aneural)

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16
Q

What causes pain in OA?

A
  • Stressors around the joint e.g. ligaments, tendons, synovial lining (neural)
  • So may be biomechanic changes that drive a lot of the pain
  • Fits that there is a v poor correlation between the extent of the radiography damage and symptoms
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17
Q

Describe the pain in OA

A
  • Typically exacerbated by activity and relieved by rest
  • With more advanced disease, pain occurs with progressively less activity, eventually occurring at rest and at night
  • Pain becomes continuous esp. hip and knee pain and even simple movements become v uncomfortable
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18
Q

What symptom other than pain is common in OA?

A

Inactivity gelling

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19
Q

Describe inactivity gelling in OA

A
  • Due to the lack of activity at night, patients will wake up and joints will be stiff (rather than RA where stiffness wakes them up and is due to diurnal variation in cortisol)
  • Morning stiffness typically lasts < 30 minutes (15-20) - shorter than RA
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20
Q

Describe the classic distribution of OA

A
  • Predilection for fingers, hands, knees, hips and spine (lower cervical and lower lumbar - spares thoracic)
  • Less commonly affects elbows, wrists or ankles (but can affect any joint)
  • DIP joint is more likely to be involved than in RA (also in PsA)
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21
Q

What would you find on examination of RA joints?

A

1) Joint tenderness
2) Bony enlargement/swelling
3) Effusions esp. noticeable at knee joint
4) Crepitus
5) Heberden’s nodes at DIP (osteophytes)

22
Q

What is different about swelling in OA than RA?

A

When you palpate the joints the swelling around the joint is bony unlike in RA where the swelling can be synovial hypertrophy and soft tissue based swelling

23
Q

Describe effusions in OA

A
  • May find the knees have a moderate amount of fluid
  • Effusions are usually cool to the touch unlike in gout/RA where joint fills with fluid and gives off heat (hot, angry red swollen joint)
24
Q

What is crepitus in the joint?

A
  • When you get the joint to move, may feel here is debris in the joint
  • This is felt as a crunching/crepitus (creaking/cracking within the joint)
25
Q

What are the radiographic features of osteoarthritis?

A

1) Joint space loss - due cartilage degradation and loss (primary pathology)
2) Joint line (subchondral) sclerosis
3) Osteophytes
4) Subchondral cysts

26
Q

What is joint line (subchondral) sclerosis?

A

When joint lines either side of the joint space (articular margins) become whitened and hardened

27
Q

What are osteophytes?

A

Bony spurs that appear around the joint margins

28
Q

What are subchondral cysts?

A
  • Subchondral bone that develops cysts

- Bony cysts that occur in the layer below the cartilage

29
Q

Although the wrist is rarely involved, which joint is commonly involved, especially on the dominant hand as it is used a lot?

A

Thumb base (CMC)

30
Q

What is a classic sign for OA in someone who has used their hand?

A

Subchondral sclerosis under the trapezium and the trapezoid as well as CMC joint disease (thumb side)

31
Q

Why can you not see the pisiform on an x ray?

A

It is hidden under the triquetrium

32
Q

Which two bones are hard to distinguish on an x ray?

A

Trapezium and the trapezoid

33
Q

How would joint space look on a knee with OA?

A

One side may have a clear gap which would be normal and the other side the gap will be gone due to loss of cartilage and the bony surfaces are touching each other and whitened

34
Q

What would a hip joint look like with OA?

A

V distorted and white with lots fo additional bone growth and cystic change, no joint line

35
Q

What is a secondary complication of OA (in the hip)?

A

Vascular necrosis

36
Q

Describe vascular necrosis

A
  • Femoral head has almost flattened off
  • Cysts in the acetabulum, pelvis and femur are much more marked
  • Femur head has collapsed
  • Important differential of OA bc if picked up early sometimes surgical interventions can prevent progression here
37
Q

What are the (limited) treatment options for OA?

A

1) Weight loss
2) Physiotherapy
3) Pain relief
4) Joint replacement

38
Q

Describe physiotherapy for OA

A
  • Good for symptom control but doesn’t alter the long term progression of OA
  • Involves range of motion and isometric strengthening
39
Q

Describe weight reduction as a treatment for OA

A
  • Reduces symptoms of OA and slows progression of the bony changes
  • Diet, behavioural interventions and physical activity
  • Exercise is hard bc of pain however diet and behavioural interventions e.g. weight watchers alone are almost just as effective
  • So if someone says they can’t exercise, don’t need to push it
40
Q

What interventions aren’t v successful in treating OA?

A
  • Lateral wedge insoles don’t help lateral compartment knee OA
  • Rest is good short term but not long term
  • TENS (transcutaneous electrical nerve stimulation)
  • Knee braces uncomfortable so people don’t want to wear them
  • Dietary interventions e.g. chondroitin or glucosamine alone have not been shown to be of benefit
41
Q

How should you treat OA with pain relief?

A
  • Analgesic ladder, start with topicals (good for local joint pain)
    1) Topicals (capsaicin)
    2) Paracetamol
    3) NSAIDs/Cox 2
    4) Intra-articular steroid
42
Q

What is the problem with pain relief in RA and why should you be cautious with it?

A
  • OA pain won’t get any better so if start pain relief will be on it for a long time so the potential for drug side effects is substantial
  • Should use the lowest level of pain relief that you can for the shortest amount of time possible and not depend on long term pain relief e.g. opiates
43
Q

What are the long term side effects of opiates?

A
  • Increased falls
  • Constipation
  • Lower QoL
44
Q

Describe use of intra-articular steroid for OA

A
  • Short term relief

- Repeated intra-articular steroid can be chondrotoxic (damage cartilage)

45
Q

What should you do when prescribing NSAIDs?

A

1) Co-prescribe PPI with NSAIDs/Cox2 to protect against gastric effects
2) Caution with use of NSAIDs alongside low dose aspirin
3) Avoid using long term (cardiac)

46
Q

What drugs should you not prescribe?

A

1) Glucosamine or chondroitin

2) Intra-articular hyaluronan (expensive and not much better than steroid)

47
Q

Describe arthroscopy/joint wash out

A
  • Short term symptomatic benefits only
  • Not superior to either sham procedure or physiotherapy
  • Not really used anymore
48
Q

When would you refer OA patients for surgery?

A
  • When OA is having an impact on QoL despite non-surgical treatment e.g. when have to change ADLs bc of symptoms
  • Refer before there is prolonged and established functional limitation and severe pain
  • Ideally want to refer before they have damage that has caused too much atrophy of the surrounding muscles e.g. quads in knee OA bc not using muscles due to pain - after surgery lots of effort with PT to get muscle strength back
  • Patient-specific factors should not be barriers to referral e.g. age, sex, smoking, obesity and co-morbidities (in the end might not be safe but still refer)
  • Not based on radiographic or other scoring tools
49
Q

What is the surgery done in OA?

A

Joint replacement (VTE risk = 1%, 1 year mortality = 0.5%, low)

50
Q

What is the primary indication for joint replacement?

A

Pain relief

51
Q

Describe the 10 year survival of the joint replacement and the effect of this on when you do surgery

A

1) In < 55 it is 83%
- Esp. relevant replace a joint that then use a lot, the replacements are not as long lasting, so the joint replacement needs to be revised
- Therefore, esp. for knees and hips try to delay surgery until people are > 55-60, don’t want to replace the joint too early
2) > 70 = 90% of joint replacements will last for well over 10 years, beyond the lifetime of the recipient

Stage 2: Ageing (10 decks)

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