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Physiotherapy in Ageing > Osteoarthritis > Flashcards

Osteoarthritis Flashcards

1
Q

What process loop/s is/are associated with acute diseases?

A

Inhibitory loop

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2
Q

What process loop/s is/are associated with chronic diseases?

A

Inhibitory loop

Auto-amplifying loop

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3
Q

What are the risk factors for rheumatoid arthritis?

A
  • Genetic factors
  • Positive for IgM and IgM rheumatoid factors
  • Varied inflammatory cascades
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4
Q

What are the impairments associated with rheumatoid arthritis?

A
  • Synovial inflammation
  • Articular cartilage damage
  • Bone erosion
  • Internal organ damage
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5
Q

What causes rheumatoid arthritis?

A

An overproduction of tumour necrosis factor (TNF)

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6
Q

What causes the synovitis associated with rheumatoid arthritis?

A

Joint if infiltrated by:

  • Increased number of fibroblast like synoviocytes
  • Increased number of macrophage like synoviocytes
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7
Q

What differences exist between +ve RA factor and +ve auto-antibody patients, and +ve RA factor and -ve autoantibody?

A

+ve RA, +ve antibody:
- More lymphocytes (B and T cells) in the synovial tissue
- More joint damage
- Fewer remissions
+ve RA, -ve antibody:
- More fibrosis and increased thickness of synovium

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8
Q

What are the clinical symptoms of RA?

A
  • Joint swelling
  • Pain/stiffness (am, <1hr)
  • Weakness
  • Deformity
  • Fatigue
  • Malaise
  • Fever
  • Weight loss
  • Depression
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9
Q

What are the articular characteristics of RA?

A
  • Palpation tenderness
  • Synovial thickening
  • Effusion (early)
  • Erythema (early)
  • Decreased ROM (late)
  • Ankylosis (late)
  • Subluxation (late)
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10
Q

What is the common distribution of RA?

A
  • Symmetrical

- Distal more commonly than proximal i.e. PIP, MCP, wrist, ankle

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11
Q

What is the common distribution of RA?

A
  • Symmetrical

- Distal more commonly than proximal i.e. PIP, MCP, wrist, ankle

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12
Q

Definition of osteoarthritis

A

A disorder involving movable joints characterised by cell stress and extracellular matrix degradation initiated by micro- and macro-injury that activates maladaptive repair responses including pro-inflammatory pathways of innate immunity

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13
Q

What characteristics are associated with OA?

A
  • Cartilage degradation
  • Bone remodelling
  • Osteophyte formation
  • Joint inflammation
  • Loss of normal joint function
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14
Q

Where does articular cartilage receive its nutrients from?

A

Synovial fluid

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15
Q

What causes the failed recovery of articular cartilage?

A

Stress

  • Genetics
  • Overload
  • Instability
  • Trauma
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16
Q

What are the risk factors of OA?

A
  • Age
  • Family history/genetics
  • Obesity
  • Gender
  • Occupation
  • Abnormal joint shape
  • Limb alignment
  • Joint trauma (fractures, instability)
17
Q

What two aspects do risk factors of OA contribute to?

A
  • Susceptibility of the joint (systemic factors or factors in the local joint environment)
  • Increased load
18
Q

What are the clinical features of OA?

A
  • Joint pain/ache
  • Morning stiffness <30 mins
  • Joint swelling
  • Decreased ROM
  • +/- crepitus
  • +/- joint line tenderness
  • +/- joint deformity
  • weakness/atrophy
19
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)
20
Q

What are the two major load-bearing macromolecules in articular cartilage? How do they work together?

A
  • Collagens
  • Proteoglycans
    The interaction between the highly negatively charged cartilage proteoglycans and type II collagen provides the compressive and tensile strength of the tissue.
21
Q

What articular cartilage changes are present with OA?

A
  • Disorganisation of articular cartilage
  • Oedema (of cartilage)
  • Chondrocyte apoptosis
  • Tide line undulation
  • Cartilage loss
  • Change in collagen type and reduction of aggrecan
22
Q

What subchondral bone changes are present with OA?

A
  • Thickening

- Osteoclast resorption and osteoblast bone formation

23
Q

What is subchondral bone thickening called when seen on x-ray?

A

Sclerosis

24
Q

At what stage may OA be somewhat reversible?

A

There is a momentary increase in the cartilage turnover in response to initial cartilage damage in the first stage of OA development, which may be reversible.

25
Q

What are Matrix metalloproteinases (MMPs)?

A

A group of enzymes that in concert are responsible for the degradation of most extracellular matrix proteins during organogenesis, growth and normal tissue turnover

26
Q

What functional outcome measures can be used for assessing knee OA?

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

What functional outcome measures can be used for assessing hip OA?

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

What functional outcome measures can be used for assessing ankle OA?

A
  • Foot and ankle score
29
Q

What performance outcome measures can be used for assessing knee and hip OA?

A
  • Stair climb
  • 6MWT
  • Gait analysis
  • Strength
  • 30s chair test
  • TUG
30
Q

What are the OARSI guidelines for non-surgical management of knee OA?

A
  • Land-based exercise
  • Weight management
  • Strength training
  • Water based exercise
  • Self-management and education
31
Q

What are the principles of physiotherapy treatment for OA?

A
  • Unload affected site
  • Correct/adjust biomechamics to change loading pattern
  • Strengthen surrounding muscles
  • Improve control/proprioception
  • Pain relief
  • Lifestyle modification
32
Q

What are the principles of physiotherapy treatment for OA?

A
  • Unload affected site
  • Correct/adjust biomechamics to change loading pattern
  • Strengthen surrounding muscles
  • Improve control/proprioception
  • Pain relief
  • Lifestyle modification

Physiotherapy in Ageing (17 decks)

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