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Flashcards in Equine MSK diseases 6 Deck (24)
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Outline the compositional changes that occur within the equine tendon as a result of exercise and age

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


Briefly outline the proposed mechanism for soft tissue ageing

- 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


What are the 4 phases of tendonopathy?

- Subclinical
- Inflammation
- Repair
- Remodelling


Describe the clinical signs of the acute inflammatory phase in tendonopathy

- Days
- Lameness
- Pain on palpation
- Heat
- Swelling


Describe the pathology that underlies the acute inflammatory phase in tendonopathy

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


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

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


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

- Angiogenesis
- Fibroplasia: ++ fibroblasts, collagen III, small collagen fibrils formed
- Reduction in space within tendon


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

- Tendon size decreases
- Tendon less pliable
- Reduce fetlock extension
- May get contractures


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

- Collagen transformation from III to I
- Cross linking
- Thicker collagen fibrils


Compare healed vs. normal tendon and the consequences of this

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


What is the prognosis for superficial digital flexor tendonitis?

Often career ending, even with stem cell therapy


Describe the normal process of tendon adaptation

- 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


Discuss the use of ultrasonography in the assessment of tendonopathy

- 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


List the factors that lead to tendonitis in the horse

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


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

- 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


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

- 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)


Outline the treatment in the subacute phase of tendonopathy

- 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)


List the treatment options available for tendonitis

- Stem cells
- Platelet rich plasma
- Bone marrow aspirates


Discuss the use of stem cells in the treatment of tendonitis

- 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


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

- 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


Outline how tendonitis in the horse can be prevented

- 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)


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

- Plantar annular ligament desmitis
- SDFT tendonitis
- DDFT tendonitis
- Suspensory ligament famage
- Tenosynovitis
- Navicular syndrome


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

- Laminitis
- Infection (sole or white line)
- Sole bruising
- Fractures


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

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