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Physio in the Ageing > OA of the Knee & Spine > Flashcards

OA of the Knee & Spine Flashcards

1
Q

What is RA?

A
  • Group of inflammatory disorders, highly variable phenotype
  • Local & systemic inflammation
  • Results in connective tissue & internal organ damage
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2
Q

What are the risk factors for RA?

A
  • 50% of risk (genetic factors)
  • Different inflammatory cascades lead to common pathway
  • 50% to 80% +ve (IgM & IgA = Rheumatoid factors)
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3
Q

What are the impairments in RA?

A
  • Synovial inflammation
  • Joint destruction
  • Articular cartilage damage
  • Bone erosion
  • Internal organ damage
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4
Q

How are chronic diseases different from acute diseases in terms of feedback loops?

A

Acute diseases:

  • Negative feedback loop
  • Initiator&raquo_space; immune inflammatory response&raquo_space; inhibitory loop

Chronic diseases:

  • Positive & negative feedback loops
  • As above +
  • Immune inflammatory response&raquo_space; damage/apoptosis&raquo_space; autoamplifying loop
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5
Q

What is the pathophysiology of RA?

A
  • Over production of tumour necrosis factor (TNF)
  • Overproduction of pro-inflammatory cytokines in synovium (synovitis)
  • Fibroblast-like cells invade the cartilage in synovium, leads to joint destruction
  • Osteoclast activation leads to joint destruction
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6
Q

What is significant about dendritic cells?

A

Most potent subset of antigen presenting cells.

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7
Q

What is the role of mast cells in RA?

A

Release histamines, inflammatory mediators & substances that promote angiogenesis and fibrosis

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8
Q

What are the two forms of RA?

A

+ve RA factor & +ve autoantibody

  • More lymphocytes in synovial tissue
  • More joint damage
  • Fewer remission

+RA factor & -ve autoantibody
- More fibrosis & increased thickness of synovium

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9
Q

Which body systems can be affected by RA?

A
  • Pulmonary: Nodules, PE, fibrosing alveolitis
  • Ocular: Keratoconjunctivitis sicca, episcleritis, cleritis
  • Vasculitis
  • Nail fold
  • Cardiac: Pericarditis, pericardial effusion, valvular heart disease
  • Neurological: Nerve entrapment, cervical myelopathy, peripheral neuropathy, mononeuritis multiplex
  • Cutaneous: Palmar erythema, pyoderma gangrenosum, vasculitic rashes, leg ulceration, amyloidosis
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10
Q

What are the symptoms of RA?

A
  • Joint swelling
  • Pain/stiffness (commonly AM >1 hr)
  • Weakness
  • Deformity
  • Fatigue
  • Malaise
  • Fever
  • Weight loss
  • Depression
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11
Q

What are the articular characteristics of RA?

A
  • Palpation tenderness
  • Synovial thickening
  • Effusion (early on)
  • Erythema (early on)
  • Decreased ROM (later on)
  • Ankylosis (later on)
  • Subluxation (later on)
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12
Q

What is the distribution of RA?

A
  • Symmetrical (especially later on)
  • Distal more commonly than proximal
  • PIP, MCP/MTP, wrist/ankle more commonly than elbow/knee, shoulder/hip
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13
Q

What is OA?

A
  • Failure of the recovery of articular cartilage from stress

- Caused by genetics, overload, instability, trauma

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14
Q

What are the risk factors for OA?

A
  • Age
  • Family history/genetics
  • Obesity (in knees, load & inflammation)
  • Sex (F)
  • Occupation
  • Abnormal joint shape
  • Limb alignment (knee valgus/varus)
  • Joint trauma (major or minor repeated)
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15
Q

Where does articular cartilage get its nutrients from?

A

Synovium

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16
Q

What are the systemic factors affecting joint vulnerability in OA?

A
  • Increased age
  • Female gender
  • Racial/ethnic factors
  • Genetic susceptibility
  • Nutritional factors
17
Q

What are the intrinsic factors affecting joint vulnerability in OA?

A
  • Previous damage
  • Bridging muscle weakness
  • Increasing bone density
  • Malalignment
  • Proprioceptive deficiencies
18
Q

What are the loading factors affecting joint vulnerability in OA?

A
  • Obesity

- Injurious PA

19
Q

What are the clinical features of OA?

A
  • Joint pain/ache
  • Morning stiffness <30mins
  • Joint swelling
  • ROM
    +/- crepitus
    +/- Joint line tenderness
    +/- Joint deformity
  • Bony enlargement
  • Weakness/atrophy
20
Q

What are the imaging features of OA?

A
  • Loss of joint space
  • Subchondral bone sclerosis
  • Para-articular cysts/spurs
  • Bone scan: hot spots (bone inflammation)
21
Q

What is the distribution of OA?

A
  • Knee/Hip
  • 1st MTP/ CMC
  • Cx and Lx (less common Thx)
22
Q

What is OA characterised by?

A
  • Disorganisation of articular cartilage
  • Oedema (of cartilage)
  • Chondrocyte apoptosis
  • Tide line undulation
  • Cartilage loss
  • Change in collagen type and reduction of aggrecan
23
Q

What are the subchondral bone changes in OA?

A
  • Thickening

- Osteoclast resorption & osteoblast bone formation

24
Q

What is the effect of anti-resorptive drugs (e.g. biophosphonates) in OA?

A

Positive effect on cartilage & bone degeneration

25
Q

What are the characteristics of each stage of OA?

A
  • Very early: Superficial lays loss & structural changes
  • Early: Internal structure changes & fibrillation
  • Moderate: Loss of organisation & hypertrophy
  • Late: Cartilage loss & denudation
  • End: Sclerosis
26
Q

What functional scores are used to assess OA of the knee?

A
  • KOOS
  • Oxford knee score
  • LEFS
  • TUG
27
Q

What functional scores are used to assess OA of the hip?

A
  • HOOS
  • Oxford hip score
  • LEFS
  • TUG
28
Q

What functional scores are used to assess OA of the ankle?

A

Foot and ankle score

  • Symptoms
  • Pain
  • ADL
  • Sport and rec
  • QoL
29
Q

What functional scores are used to assess OA of the spine?

A
  • Not a clear set of PROM

- A pain score, a QoL score and pathology (e.g. ODI, Roland Morris) score

30
Q

What performance scores are used to assess OA of the knee & hip?

A
  • Stair climb
  • 6 mwt
  • Gait analysis (4 x 10mwt)
  • Strength
  • 30 second chair test
  • TUG
31
Q

What are the core treatments for knee OA according to the OARSI guidelines?

A
  • Land-based exercise
  • Weight management
  • Strength training
  • Water-based exercise
  • Self management & education
32
Q

What are the principles of physio treatment for OA?

A
  • Unload affected site (weight management, SPS)
  • Correct biomechanics (orthotics, gait retraining)
  • Strengthen muscles
  • Improve control & proprioception
  • Pain relief
  • Life style modification (Change of exercises, learn what aggs, coaching)
33
Q

What treatments should not be given for OA?

A
  • Electrotherapy
  • Avocado soybean
  • Chondroitin +/-
  • Glucosamine
  • Acupuncture
  • Opioids (largely uncertain)
  • Knee arthroscopies
34
Q

What is spinal spondylosis?

A
  • Diagnosed by XR
  • 3 joint pathology (disc space narrowing, facet degeneration, osteophytes)
  • Disc space narrowing appears to be initiator of spondylosis
35
Q

What are examples of spondylosis being different from OA?

A
  • Facet joint OA can be present without DSN
  • Osteophytes can form without cartilage association
  • DSN common in ageing
  • Facet OA associated with knee & hand OA, but not DSN
36
Q

What are the risk factors for spondylosis?

A
  • Association between osteophytes or DSN & LBP is modest
  • Osteophytes appear earlier than DSN and FOA
- OA changes modest association with LBP
  • DSN progression associated with hip/knee OA
37
Q

What interventions should be used to treat OA in a 40yo?

A
  • Keep weight down
  • Strength, flexibility, protection
  • Moderate exercise
  • Avoid injury
  • Avoid surgery
38
Q

What interventions should be used to treat OA in a 70yo?

A
  • ROM
  • Stretching
  • Proprioception and balance
  • Falls prevention
  • Strengthening for stabilisers
  • Treatment of gait adaptations
  • Education of how to manage
  • Joint replacement

Physio in the Ageing (10 decks)

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