Diagnostics Equine Musculoskeletal (Renate) Flashcards

1
Q

Waht are the big 7 in orthopaedic disease complexes in horses?

A
  1. OA
  2. OCD
  3. Fx (fatigue or impact)
  4. Tendonitis
  5. Navicular dz
  6. Wounds
  7. Laminitis
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2
Q

Why are some iaging modalitis chosen over others in horse?

A

Need for GA - 1% death risk for hroses is a big deal!

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3
Q

What type of image do radiographs produce?

A

“summation image”

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4
Q

Other names for OA

A
  • arthrosis, DJD
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5
Q

What are osteophytes? What similar structures are seen elsewhere?

A

> New bone fomation along the ‘lip’ edges of articular surface (trying to stabilise the joint)
Inthesiophytes = new bone formation at attachement of a soft tissue structure

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6
Q

Can cartilage be seen on rads?

A

NO - just see narrowed/widened join space

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7
Q

What is high ringbone?

A

OA of the pastern joint -> MINIMAL synovial response, straight to swelling d/t palpable bony changes above the coronary band

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8
Q

Outline the stages of pathogeneis assocaited with OA

A
  1. joint effusion (bog spavin in the hock)
    - excessive synovial fluid d/t irritation and inflammatio nof the synovial membrane
  2. cartilage damage
  3. boney damage
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9
Q

How do horses IVDs differ to smallies?

A

No nucleus pulposus (only fibrous tissue) so dont get disk problems

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10
Q

How are the 3 main stages of damage associated with OA visable on rads?

A
  1. joint effusion and osteophytes
  2. articular artilage: narrowed joint space
  3. subchondral bone: sclerosis/lucency (lucency worse prognostically as body given up -> lysis)
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11
Q

Wht may narrowing of the joint eventually lead to?

A

Ankylosis

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12
Q

What is surgical ankylosis termed? How is this performed?

A

Arthrodesis

  • chemical/physical destruction of cartilage
  • only possible in low motion joints eg. DIT and IT joints mainly for shock absorption not movement
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13
Q

What is bone spavin?

A

OA of the DIT and IT joints -> ankylosis

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14
Q

Gol standard diagnostic method for OA?

A

MRI

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15
Q

What is prognosis and tx after dx based on?

A

> structures affected (high v low motion joints)
type of disease (1/2, traumatic, devlopmental)
advanced disease? (early v late stage)

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16
Q

How does inflamed synovial fluid appear cf. healthy?

A

decreased viscosity (MORE watery!!!)

17
Q

What are corns?

A

Inflammation of a specific area of hoof wall (dx with hoof testers and hoof knife, easy - shouldnt get to referral stage to be dx wih corns!)

18
Q

Tx stategies for OA?

A
  • strategic analgesia
  • joint supplements
  • novel tx concepts
  • salvage procedures
  • excercise modification/physio
19
Q

What cause the changes in synovial fluid composition when inflamed?

A
  • PGE2 and MMPs: V proteoglycans, ^ water and ^ collagen breakdown
  • IL1 and TNFa
  • PG, LT, free radicals and neuropeptides
20
Q

Where do steroids and NSAIDs act?

A

> steroids PLA2
- cell membrane phospholipid -> arachadonic acid stage
NSAIDs COX
- arachadonic acid -> PGs and Thromboxanes
- 5-lipoxygenase pathway -> leukotrienes
pain,swelling and cartilage degradation, heat (inflammation)

21
Q

Prevention of OA?

A
  • v BCS
  • shoeing and correct foot shape
  • other things…
22
Q

Look up aetiology/pathogenesis, clinical signs, imaging signs, Dxx, Dx, Prog and Tx of all the big 7

A

~~~~

23
Q

Most common site of lameness in the horse?

A
  • foot (difficult to relate pain o secific structures by direct visualisation, palpation or manipuplation)