Week 2 - Mobilisation - reduced ROM Flashcards

1
Q

What are the structures that normal movement is dependent on?

A
  • Ligaments (periarticular)
  • Capsule (periarticular)
  • Cartilage (intraarticular)
  • Tendons
  • Fascia
  • Synovium (intraarticular)
  • Muscles (extra-articular)
  • Skin (extra-articular)
  • Bone
  • Subcutaneous tissue
  • Neurological control
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2
Q

What may dysfunction of these structures lead to?

A

Dysfunction of any of these structures can lead to abnormal or reduced joint movement.

Reduced movement can lead to abnormalities in these structures.

Normal movement is necessary to maintain the functions of these structures.

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3
Q

What may abnormal joint movement involve?

A

Reduced range of movement
Hypermobility
Insufficient neurological control

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4
Q

What does reduced range of movement involve?

A
  • Reduced range of passive motion
  • Stiffness/hypomobility/contracture
  • Decreased ROM
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5
Q

What does hypermobility involve?

A
  • Increased range of passive/active motion
  • May be desirable, pathological or incidental
  • Without sufficient muscle control can lead to joint instability
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6
Q

What does insufficient neurological control involve?

A
  • Muscle tone and/or control around joints abnormal
  • Usually pathological
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7
Q

What does contracture mean?

A

Irreversible reduced range of passive movement

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8
Q

Cells in connective tissue?

A

Fibroblasts - maintain exc matrix
(chondroblasts and chondrocytes in cartilage )

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9
Q

What is the extracellular matrix made up of?

A

Fibres → elastin, reticulin, collagen - pre-dominant

Ground substance → water, proteoglycans, GAGs

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10
Q

Key points about collagen?

A

→ Is being continuously turned over - continually synthesised by fibroblasts and degraded by enzymes

→ Synthesis of collagen stimulated by tensile loading - comes from normal movement (stress/strain)

→ Layed down parallel to lines of stress it withstands

Shows why normal activity is essential to the homeostasis of joint structures.

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11
Q

What determines joint ROM?

A

→ The structure of the joint itself (arthrology)

→ Resistance within the joint - normally incredibly low co-efficient of friction due to lubrication of cartilage by synovial fluid + proteoglycan called lubricin

→ The properties of each joint structure (intra, peri and extra-articular)

→ How external forces are transmitted by the articular soft tissue (passive viscoelasticity)

→ Varying concentrations of the following determine viscoelastic properties and response to lengthening:
- elastin, collagen, proteoglycans and water

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12
Q

Mechanical properties of articular connective tissues?

A
  • Dense connective is very strong - parallel bundles of collagen fibres
  • Organised structure
  • Resistant to tensile stress = stiff
  • Strongly resistant (rope-like) along lines of stress - long axis
  • Tendon (most stiff) > Ligament > Joint capsule strength
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13
Q

Define stiffness

A

The ability to resist tensile stress - desirable quality at tissue level

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14
Q

Mechanical principles of connective tissues?

A

Crimping of collagen fibres
Viscoelasticity

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15
Q

What does the crimping of collagen fibres involve?

A
  • Gives collagen fibres wavy appearance under microscope
  • Only small force required to produce large initial elongation in the structure

One the crimps have straightened, the elongation is proportional to the applied force

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16
Q

What is microfailure?

A

When force and elongation continue to increase
Small tissue tears occur.
May result in permanent change to structure’s length.

CALLED PLASTIC DEFORMATION

In healthy tissues, the force needed to cause this are really high and associated with a rapid/high force incident e.g. football tackle

17
Q

What is rupture?

A

Even greater force.
Rupture of entire structure.

In healthy tissues, the force needed to cause this are really high and associated with a rapid/high force incident e.g. football tackle

18
Q

What is creep?

A

Load on tissue maintained over time
Tissue gradually elongates a little bit more over time

Part of the reason for holding a stretch

19
Q

What is stress relaxation?

A

If you elongate tissues and continue to elongate them, The stress of the tissue reduces

Supports the need to sustain a stretch

At least 30s of sustained loading is required to effect a permanent change in the length of established connective tissue.

20
Q

Causes of reduced range of movement?

A

Trauma
Immobility
Chronic disease

21
Q

Examples of trauma (traumatic injury)

A
  • fractures
  • muscle strains
  • sprains
22
Q

Why may immobility occur?

A
  • hospital
  • nursing home
  • older persons
23
Q

Example of chronic disease?

A
  • osteoarthritis
  • rheumatoid arthritis
  • neuromuscular disorder
24
Q

Examples of trauma and immobility combined

A
  • plaster cast
  • bed rest
25
Q

Examples of trauma and chronic disease combined

A

joint replacement
brain injury

26
Q

Examples of chronic disease and immobility combined

A

chronic pain
cardiorespiratory disease

27
Q

Effects of reduced range of movement

A

→ Function - UL - reduced independence with functional tasks - LL - poor gait and functional mobility, falls risk

→ Pain

→ Muscle weakness

→ Vicious circle of inactivity

28
Q

What is the vicious cycle of reduction in ROM?

A

Reduced ROM → Reduced function → Deconditioning → Decreased motivation → Decreased activity →

29
Q

Physiological changes of immobility on connective tissue?

A

Immobility → stress deprivation → remodelling

Without stresses and strains of everyday activities, remodelling of the tissue occurs.

30
Q

Early physiological changes of immobility?

A

→ Decreased collagen
→ Decreased GAGs and water content
→ Decreased alignment of collagen fibres
→ Decreased crosslinks between collagen fibres (no longer parallel w/stresses

= shorter
= weaker
= decreased resistance to tensile stress

31
Q

Late physiological changes of immobility?

A

→ fibroblast proliferation
→ myofibroblasts
→ fibroblasts produce dense, disorganised collagen fibrils → myofibrils shorten structures further, resulting in:

  • adhesions, fibrocartilage and ossification (fixed contracture - take weeks/moths to develop)
32
Q

How is a fixed contracture resolved

A

Only resolved with surgery

33
Q

How do physiological changes due to immobility change if a tissue injury is also present? e.g. knee sprain

A

Too painful to move joint.
Inflammatory responses associated with soft tissue healing as well as changes caused by immobility.

HOWEVER more emphasis on….
→ cellular proliferation earlier
→ more significant myofibroblast activity

Thus effects of healing compounded by the immobility and vice versa.

34
Q

How does immobility/injury change the structure of connective tissue?

A

From strong rope-like structure to net structure.

→ Disorganised with some perpendicular fibres
→ Weaker overall structure
→ Weakly resistant in all directions
→ Resists movement in multiple planes

Although structure e.g. lig. is weaker and less stiff, the joint ROM is reduced

35
Q

Negative effects of immobility on cartilage?

A

↓ water content
↓ GAGs
↓ nutrients from synovial fluid
↓ thinning of extracellular matrix
↓ fibro-fatty connective tissue proliferation
↓ adherence of synoviocytes and protein deposits (making it less smooth and more resistant to movement)

36
Q

Negative effects of immobility on synovium?

A

↓ no of synoviocytes
↓ synovial fluid volume
↓ synovial fluid movement (loss of “sweep and squeeze”
↓ lubricin (lubrication)
↓ adhesions between micro-folds in synovial membrane

37
Q

Negative effects of immobility on bone?

A

↑ resorption of both cancellous and compact bone (after approx 8 weeks)
↓ bone mineral density (BMD)
↓ ability to withstand stress - increased risk of fracture with excessive force

38
Q

Negative effects of immobility on muscle?

A

atrophy

sarcomeres lost from end of myofibrils = shortening

connective tissue proliferation → increased collagen within endomysium, perimysium + epimysium = adaptive shortening (more connective tissue in muscle compared to myofibrils after immobility).

muscle shortening = most significant limitation to joint range in healthy individuals

39
Q
A