Diagnostics Equine Musculoskeletal (Renate) Flashcards
Waht are the big 7 in orthopaedic disease complexes in horses?
- OA
- OCD
- Fx (fatigue or impact)
- Tendonitis
- Navicular dz
- Wounds
- Laminitis
Why are some iaging modalitis chosen over others in horse?
Need for GA - 1% death risk for hroses is a big deal!
What type of image do radiographs produce?
“summation image”
Other names for OA
- arthrosis, DJD
What are osteophytes? What similar structures are seen elsewhere?
> 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
Can cartilage be seen on rads?
NO - just see narrowed/widened join space
What is high ringbone?
OA of the pastern joint -> MINIMAL synovial response, straight to swelling d/t palpable bony changes above the coronary band
Outline the stages of pathogeneis assocaited with OA
- joint effusion (bog spavin in the hock)
- excessive synovial fluid d/t irritation and inflammatio nof the synovial membrane - cartilage damage
- boney damage
How do horses IVDs differ to smallies?
No nucleus pulposus (only fibrous tissue) so dont get disk problems
How are the 3 main stages of damage associated with OA visable on rads?
- joint effusion and osteophytes
- articular artilage: narrowed joint space
- subchondral bone: sclerosis/lucency (lucency worse prognostically as body given up -> lysis)
Wht may narrowing of the joint eventually lead to?
Ankylosis
What is surgical ankylosis termed? How is this performed?
Arthrodesis
- chemical/physical destruction of cartilage
- only possible in low motion joints eg. DIT and IT joints mainly for shock absorption not movement
What is bone spavin?
OA of the DIT and IT joints -> ankylosis
Gol standard diagnostic method for OA?
MRI
What is prognosis and tx after dx based on?
> structures affected (high v low motion joints)
type of disease (1/2, traumatic, devlopmental)
advanced disease? (early v late stage)
How does inflamed synovial fluid appear cf. healthy?
decreased viscosity (MORE watery!!!)
What are corns?
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!)
Tx stategies for OA?
- strategic analgesia
- joint supplements
- novel tx concepts
- salvage procedures
- excercise modification/physio
What cause the changes in synovial fluid composition when inflamed?
- PGE2 and MMPs: V proteoglycans, ^ water and ^ collagen breakdown
- IL1 and TNFa
- PG, LT, free radicals and neuropeptides
Where do steroids and NSAIDs act?
> 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)
Prevention of OA?
- v BCS
- shoeing and correct foot shape
- other things…
Look up aetiology/pathogenesis, clinical signs, imaging signs, Dxx, Dx, Prog and Tx of all the big 7
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Most common site of lameness in the horse?
- foot (difficult to relate pain o secific structures by direct visualisation, palpation or manipuplation)