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MSK2 > Equine MSK diseases 6 > Flashcards

Equine MSK diseases 6 Flashcards

1
Q

Outline the compositional changes that occur within the equine tendon as a result of exercise and age

A
  • Decrease in GAG
  • Alteration in Cartilage Oligomeric Matrix Protein (COMP) which acts to accelerate collagen fibril formation i.e. is organisation molecule
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2
Q

Briefly outline the proposed mechanism for soft tissue ageing

A
  • Cyclical load on cells either leads to matrix synthesis/repair (immature tendon), or MMP production (aged tendon)
  • MMP prod → reduction of ultimate tensile strength, and matrix resorption → matrix protein fragmentation → load on cells
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3
Q

What are the 4 phases of tendonopathy?

A
  • Subclinical
  • Inflammation
  • Repair
  • Remodelling
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4
Q

Describe the clinical signs of the acute inflammatory phase in tendonopathy

A
  • Days
  • Lameness
  • Pain on palpation
  • Heat
  • Swelling
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5
Q

Describe the pathology that underlies the acute inflammatory phase in tendonopathy

A
  • Haemorrhage

- Inflammation: neutrophils, macrophages, monocytes, increased blood flow, oedema, proteolytic enzymes

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6
Q

Describe the clinical signs of the reparative (subacute) phase of tendonopathy

A

Weeks, overlaps with acute phase

  • Reduce or absence of lameness
  • Resolution of signs of inflammation
  • Tendon still palpably enlarged and soft
  • Signs of re-injury if exercised too early
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7
Q

Describe the pathology that underlies the reparative (subacute) phase of tendonopathy

A
  • Angiogenesis
  • Fibroplasia: ++ fibroblasts, collagen III, small collagen fibrils formed
  • Reduction in space within tendon
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8
Q

Describe the clinical signs of the remodelling (chronic) phase of tendonopathy

A

Months

  • Tendon size decreases
  • Tendon less pliable
  • Reduce fetlock extension
  • May get contractures
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9
Q

Describe the pathology that underlies the remodelling (chronic) phase of tendonopathy

A
  • Collagen transformation from III to I
  • Cross linking
  • Thicker collagen fibrils
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10
Q

Compare healed vs. normal tendon and the consequences of this

A
  • Healed is stiffer

- re-injury common, poorer performance, other tendons stretch to accomodate loads

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11
Q

What is the prognosis for superficial digital flexor tendonitis?

A

Often career ending, even with stem cell therapy

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12
Q

Describe the normal process of tendon adaptation

A
  • Load → matrix deformation
  • Tenocytes detect this and via mechanotrasnduction → cellular response
  • Enables remodelling of tendon matrix according to imposed loads
  • Matrix metalloproteins degrade the tendon matrix to allow normal matrix turnover and repair
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13
Q

Discuss the use of ultrasonography in the assessment of tendonopathy

A
  • Wait ~7 days after injury before scanning
  • Used to indicate size of lesion and treatments required
  • Can be used to establish prognosis by assessing initial severity, and fibre alignment when returns to full work
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14
Q

List the factors that lead to tendonitis in the horse

A
  • Tendon failure
  • Loss of ability to adapt and repair microdamage (ageing)
  • Tendon degeneration
  • Cumulative fatigue damage (exercise)
  • Abnormal loading events
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15
Q

Explain how abnormal loading events can lead to tendonitis, specificaylly in the SDFT

A
  • Muscle fatigue → incoordination and abnormal loading
  • Fast twitch DDFT muscle fatigues earlier → reduced MCP stabilisation → abnormal SDFT loading
  • Increased risk of tendon injury at the end of a race
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16
Q

Outline the treatment of tendonopathy in the horse in the acute phase

A
  • Anti-inflammatory in order to minimise proteolytic digestion of normal tendon around site of injury, aids with comfort
  • Physical: application of cooling, compression bandage to reduce oedema, MCP joint support, rest
  • Medical: NSAIDs, corticosteroids (early in disease)
17
Q

Outline the treatment in the subacute phase of tendonopathy

A
  • Mobilisation: early and progressive
  • Regular ultrasonographic monitoring: cross sectional area of lesion
  • Push exercise as far as possible (increased CSA = inflammation, reduce exercise. No change in CSA = no inflammation, push a little further)
18
Q

List the treatment options available for tendonitis

A
  • Stem cells
  • Platelet rich plasma
  • Bone marrow aspirates
19
Q

Discuss the use of stem cells in the treatment of tendonitis

A
  • Stem cells appear to orchestrate healing rather than synthesise matrix/becoming new tenocytes
  • Only transient cell survival
  • Aim is to make more function scar tissue and reform tendon matrix
  • Stem cell s obtained from sternum using local anaesthetic and sedation
  • Some evidence supportive of beneficial effects
20
Q

How can re-injury following SDF tendinitis be prevented? Give the prognosis for each

A
  • Desmotomy of the ALSDFT (transfers load away from SDFT). Potential for reduced rate of re-injury
  • Dalmar support boot: support to MCP joint, can be used in exercising horse but not race/event/high level jumping
21
Q

Outline how tendonitis in the horse can be prevented

A
  • Maximise quality of tendon prior to skeletal maturity (best), pasture exercise of foal ideal
  • Reduce degeneration after skeletal maturity (avoid tendon training after 2yo, used interval training, limit repetitive loading)
  • Reduce risk factors for tendonitis (e.g. speed on hard ground, incoordination, jumping, overweight, shoeing)
  • (Early detection - ultrasonography)
22
Q

List the ddx for the following clinical presentation:
- 11yo showjumper with persistent lameness of ~4months in RH, rest has done little to alleviate lameness, work exacerbates lameness. “Notch” on plantar surface at the level of metatarsophalangeal joint, substantial effusion of digital flexor tendon sheath

A
  • Plantar annular ligament desmitis
  • SDFT tendonitis
  • DDFT tendonitis
  • Suspensory ligament famage
  • Tenosynovitis
  • Navicular syndrome
23
Q

List the conditions of the equine foot that will cause heat and bounding digital pulses

A
  • Laminitis
  • Infection (sole or white line)
  • Sole bruising
  • Fractures
24
Q

List the conditions of the equine limb that are usually more lame on hard ground

A
  • Navicular disease
  • Distal interphalangeal joint disease (e.g. synovitis, degenerative joint disease, infectious arthritis, trauma/fractures)
  • Diseases of the foot

MSK2 (29 decks)

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