LOCOMOTION

what is navicular syndrome? what is the best way to diagnose it/localise it? what structures are most often involved?

"palmar heel pain". there is no one cause, distinct pathophysiology, lesion-oriented cure. DIAG: ADVANCED IMAGING MODALITIES STRUCTURES: - Navicular bone/bursa - DDFT - DIP joint or collateral ligaments of DIP joint

what are the grades of horse lameness? how do they differ?

*USA:* 0 - lameness not perceptible (AAEP) 1 - difficult to observe 3- constantly observable at a trot under all circumstances 5: minimal weight-bearing in motion UK: 0-10. 2: hard to detect at walk or trot 4: barely detectable at walk, easy at trot 6: easily detectable at walk 8: hobbling at walk, unable/unwilling to trot 10: non wt. bearing very subjective.

how to prepare a cow for foot surgery (claw amputation)? how is the surgery performed and what is the prognosis?

- AB - Analgesia - IV regional anaesthesia: IVRA. tourniquet, butterfly catheter, 20 ml procain. test interdigital space. then: - incise into interdigital space: 2-3 cm, skin fold. - embryotomy wire - up then obliquely outwards. aim to go out the far end of P1. - curette + remove any excess tissue. PRESSURE bandage because bleeding a lot. redress 48 hrs, 96hrs, 7 days, then leave open. block on unaffected digit. PROGNOSIS: not dreadful. another few years. worse for front feet, amps thru PII (as opposed to PI). survival roughly 3 years.

what are herd interventions for DD?

- Footbathing: using AB is NOT licensed as a FOOTBATH. formalin 4-5% or copper sulfate. - Slurry mgmgt - Biosecurity

what is the current diagnostic approach to navicular syndrome?

- ID of multiple structures involved in "heel pain". 1) history: BILATERAL lameness, toe ELEVATION may increase LAMENESS 2) positive response to palmar digital nerve block - advanced blocking required. DIP joint and NAV bursa 3) Hoof testers usually negative 4) correct ID of affected structures with advanced imaging modalities - combine w/ findings from diagnostic analgesia - radiograph - advanced imaging: MRI +/- CT, scintigraphy, ultrasonography 5) navicular bursoscopy (indications from diagnostic analgesia and advance imaging such as navicular bursa, DDFT tears, etc) 6) corrective farriery, controlled exercise, and pain relief 7) response to tx.

what locations of the older horse (chronic progressive osteoarthritis) are common?

- PIJ - DIJ - MPJ - carpometacarpal joint - coxofemoral joint - femorotibial joints - tarsus - previous injury (Retired racehorse)

what are the endocrine tests for laminitis horse?

- PPID: clinical signs, - basal ACTH (adjust for season) - TRH stim test EMS: history, clinical signs, demo of ID (fasting insulin, glucose)

what are non-erosive polyarthritis examples (that isn't IMPA)?

- SLE - Lyme disease (borrelia burgdorferi) - drug-associated (dobies + sulphonamides) - associated with steroid-responsive meningitis-arteritis - vaccine-induced (calicivirus kittens, distemper)

cryotherapy as physiotherapy: uses?

- affects vasculature (constriction), and nerves (analgesia) directly - can use even in non-ambulatory patient, esp. in acute tx (most effective) - abt 20 minutes can use ice packs, cryogel, ice path, vapour coolant.

how to detect a deep digital flexor tendinopathy?

- almost always within digital sheath or navicular bursa (synovial cavity). associated with swelling of those. - mid-substance disruption (image) or marginal tears leads to TENOSYNOVITIS.

what are ways and means of therapeutic shoeing?

- breakover modifications - ground surface mod of the shoe - mod. of hoof support and wt. bearing - shock absorbing shoeing - wt. reduction - hoof wall defect stabilisation often combination of means.

in a RTA, what would be your case management plan from when the patient enters?

- clinical exam/eval - first aid/emergency care - stabilisation - exam/eval limb - damage limitation: application of external skeleton fixators, woung mgmt - definitive tx: nerve repair, regen of vascular system, skin recon, repair muscles/tendons/ligaments - bone repair

how can you restrict grazing to prevent equine endocrinopathic laminitis?

- consider zero grazing for some horses (turn out with a muzzle on or turn out in the school/woodship) - turn out late night to early am (low NSC) - restrict in spring, autumn (growing) - avoid if frost with bright sunshine or drought - rotate paddocks to keep grass at appropriate height - restrict intake: muzzle, strip grazing regular exercise, prevent obesity

what is the function of hip dysplasia screening? what are its uses and limitations?

- detect carrier animals by radiographic signs - detects primary disease (ED, HD) - detects secondary osteoarthritis - has no relevance to the clinical problem however: dogs with GOOD SCORES can carry genes for very BAD HIPS. doesn't identify laxity. genetic analysis preferable - less variability.

what is the use of massage in physiotherapy?

- direct impact on tissue: pain relief - addresses decreased mobility - mechanical restriction, post-surgery, disease - preventative: athletes/performances. warm up/recover MECHANISM: genuine physiological background - relaxation - continuous touching and palpation- lowered stress, endorphins - direct activation of neuropeptide release - lymphatic flow - improved circulation USE: isolated area often (just one limb, etc). can teach owners how to do because it's time consuming, physically demanding. TECHNNIQUES: not needed

what should be done on a stifle exam of an animal with a CCL injury?

- effusions (losing clarity of edges) - medial buttress on fibrous tissue on the tibia - patellar tracking, crepitus (ROM) or can feel it/listen to it, +/- pain. STABILITY TESTS - cranial draw: most reliable. hold femur and tibia and see if the bottom can slide. some dogs won't tolerate it - need to grip tightly. repeat under sedation. can have false positive it twisting. - tibial thrust: dynamic. hold femur and push up on hock. can feel tibia go forward. better for bigger dogs, well tolerated, can do standing.

what is the process of indirect healing?

- fracture occurs: bleeding, haematoma, release of GF - bone resorption at both ends, GF release - vascularisation, organisation, differentiation, osteogenesis - development of extraosseus blood supply, periosteal/cortical callus completes scaffold linking bones together - long term remodelling

what are the risk factors for IMPA?

- genetics: beagles, nova scotia duck tolling retrievers - infections: bacterial endocarditis, discospondylitis - immune mediated bowel disease - neoplasia - chronic hepatitis

what is the approach to lameness bovine lameness?

- history as you approach, look at mobility score - restrain calmly then move quickly - establish leg OR foot IF FOOT - wash foot - dutch 5 stem trip - careful examination - decisions: prognosis cow/claw, NSAID, local exam (IVRA), apply block if claw lesion (block of wood on healthy claw to prevent weight bearing on lesion), AB, straw yard/paddock, surgery (removal of growth or claw)

what history questions should you take with a dairy cow?

- how long? - what tx (masking/worsening signs) - other foot problems before? - which lactation (heifer = alarm bells, age helps decide tx) - how long calved (fresh cow vs. stale) - is she pregnant or on the cull list (worth tx surgically?)

how do you PE a cow's foot?

- how she is placing - pain (heel bulb, gentle claw twist, thumb pressure) - heat or softening at heel/coronary band (where an abscess might be waiting to pop out) - swelling/redness/odour (foul, white line smells) - roughening - visible lesions - beware haemorrhage can be 2-3 months old by the time you spot it - hoof testers - pain, movement, noise THEN: CLEAN, FUNCTIONAL TRIM - sawdust? hose? disinfect. dutch 5 step foot trimming.

what are 3 causes of crystal induced arthritis?

- hydroxyapatitte - calcium pyrophosphate (psuedogout) - sodium urate (gout)

how is immune mediated polyarthritis treated?

- identify inciting factor and remove/treat - modify lifestyle - suppress immune response - pain relief if NB RA or multisystemic: needs more aggressive and prolonged therapy. DRUGS: - prednisolone (2-4 mg/kg daily), divided. gradually taper - +/- cytotoxic drugs: cyclophosphamide (but haemorrhagic cystitis), azathioprine (not cats), disease-modifying antirheumatic drugs - biologic agents (anti-TNFa, IL-1) - possibly empirical treatment of Lyme disease if present in area monitoring: response often within 7 days. substantial decrease in WBC is important. surgery: for pain mgmt in chronic disease

what are signalment, physical exam etc of a dog with a CCL injury?

- insidious or acute onset lameness - can have mild to severe lameness - acute ruptures are initially non-wt bearing and then can have a plateauing lameness. - may sit with leg extended and out to side - (+ve sit test) PE: - musculature/stance - spinal palpation/tail life to distinguish lumbosacral disease - stifle diagnostics: ORTHAGONAL RADIOGRAPH. can't diagnose only can see secondary changes. - stifle effusion - osteophytes: proximal/distal poles of patella, tibial plateau, trochlear ridges, fabella - distal displacement of the popliteal sesamoid bone ARTHROCENTESIS (rarely needed), MRI/contrast CT (rare)

what is a tibial tuberosity transposition?

- intra-operative assmt post trochleoplasty: straighten femur/tibia, flex/extend stifle - deviated patellar tendon suggests that it needs transposition bone: re-aligned, stabilised with pin, tension band wire. tighten lateral tissues and excise redundant tissue OR imbricate (safer as can regain length if needed). re-check patella tracking. MAY lead to abnormal distal position of insertion if YOUNG. ideally wait >10 mo or two stage - trocheoplasty + soft tissue augmentation, later TTT

what is the clinical definition of OA?

- lacks most classical signs of inflammation - pain - swelling of joint - disability, stiffness after rest - serology (IgM negative) - fibrillation + softening evident of cartilage surface - Narrowing of joint space - osteophyte formation by radiology - subchondral bone sclerosis - crepitus biochemical definition: - changes in cellular component, DNA/RNA component, and protein component

what are ground surface modification (therapeutic farriery) ? what is an example?

- most effect on penetrable ground - changes centre of ground reaction forces - prevents heel sinking however: may strain SL and SDFT in mid stance phase example: egg bar shoe with setback blunted toe. - favours sinking of toe in penetrable footing facilitating breakover, relieving DDFT

how can you assess if your OA mgmt plan is working?

- need repeatable assessments: formalising history taking (owner assisted outcome measures) - formalising physical exam - questionnaires but the scores can vary based on preceding day goniometry: manually reduced and pain/discomfort induced. semi-quantitative accelerometers: indication of activity (daytime, night-time restlessness)

ideal horse splint

- neutralises damaging forces - not too heavy (pendulum effect, further vertical distraction) - applicable under difficult circumstances (minimal asst, no anaesthesia/recovery) - economical, accessible (boards/slats, light metal rods, PVC pipes, casting material)

how should you palpate an over-strain injury of an equine tendon?

- observe swelling - palpate with both weight bearing, limb lifted - some areas difficult to palpate: proximal SL in hindlimb, pastern - assess both limbs - assess: pain on palpation, suppleness of tendons, oedema

DDx for an osteosarcoma diagnosis?

- other sarcomas (chondro-, fibro-, haemangio), -metastatic disease (prostatic carcinoma to lumbar vertebrae, would have tenesmus or ribbon-like faeces), - myltiple myeloma, lymphoma, osteomyelitis (warm climates: fungal, bacteria), bone cysts (well-demarcated)

what are the main infectious causes of ovine lameness?

- ovine interdigital dermatitis (scald) - footrot - contagious ovine digital dermatitis - contagious pustular dermatitis - strawberry footrot - toe abscess - laminitis = FMD - bluetongue

how should P3 fractures be treated? what are the goals?

- provide support: bar shoe with large side clips - limit hoof extension late bearing: rim cast - stabilise fracture: foot cast

what exercise regimen is good for dogs with OA?

- regular shorter walks vs one long walk - soft-terrain, warm ups, reduced off lead work - owner assess pain - hydrotherapy: low impact joint strengthening, resistancw rok - physiotherapy

what are the use of electrotherapy, laser, and US for physiotherapy?

- require acquisition of specific equipment - require training: on grounds of patient and operator safety. US therapy: used the most in human field. don't know very much in small animals. - heating effect: heats deeper tissues - hard to monitor - useful for soft tissue shortening, fibrosis, chronic inflammatoin, pain, etc. - tendinitis, bursitis, joint contracture, mm. main, spasm. ELECTRICAL STIMULATION: - NMES - current applied to patient that depolarises motor nerve, causes contraction. can keep muscle bulk up when the patient isn't doing anything. - increases muscle mass. LASER therapy: least amount of evidence - claimed to work on vasodilation, pain, tissue regeneration by a combo of heating, direct photostimulation effects - very difficult to monitor - need a lot of health and safety training. - helpful for wound healing. - least worth it

fractures involving the articular surface: requires what?

- requires open reduction with internal fixation (ORIF) + compression - occasionally removal fo small chips - occasionally conservative for non-wt bearing areas - if the joint cannot be appropriately fixated then consider salvage accurate anatomical reduction: recreate smooth joint surfact internal fixation with compression: engenders primary bone union (no callus), stops synovial fluid ingress SALTER classification

what are the types of erosive polyarthritis? what is the mechanism?

- rheumatoid arthritis - periosteal proliferative polyarthritis (cats) - polyarthritis of greyhounds (Felty's Sundrome) - RA, splenomegaly, neutropaenia mechanism: chronic synovitis leads to production of proliferative granulation tissue (pannus) which invades articular cartilage and can erode sub-chondral bone. - pannus + inflamed synovium produce enzymes including proteases and collagenases, leading to further destruction - similar to septic arthritis ~1% of PA Aetiology: - cellular or humoral immunopathogenic factors - release of chondrodestructive collagenases/proteases - failure of self-tolerance of production of immunogenic IgG

what are 4 breakover modifications?

- setting back show relative to toe - blunting toe of shoe - rolling ground surface of shoe in toe area - rockering toe - combo of all 4

history of a lame patient: what to ask?

- signalment (esp. ae) - trauma, duration - deterioration/improvement, circumstances - effects of exercise - type of sporting activity (horses, etc - level or competition): what is the expectation for function additional sources: - images, videos, records, imaging

what are the radiographic features of OA?

- soft tissues - dystrophic mineralisation, effusion - capsule changes - subchondral bone sclerosis

what considerations should be made before performing foot surgery in a cow?

- sound medial claw + other feet? - placing foot normally? - is she barren/should she be culled? - can the farm cope with aftercare? (soft bedding, bandage, etc)

how can you detect desmitis of the accessory ligament of the DDFT (inferior check ligament)?

- swelling in proximal metacarpal region - dorsal to the SDFT - lameness variable: often absent - ultrasonography: generalised enlargement, hypoechoic (darker)

how should you observe the gait of a lame patient? how can you determine which limb is lame?

- towards/away/across, 2 different speeds. - possibility of circling/turning to exaggerate abnormalities - decide which limb is the problem first: SINKS ON THE SOUND SIDE (head nod if thoracic limb, sinking at tarsus if pelvic limb)

what is a horse's gait (pace)? is it a problem?

- two-beat lateral gait. ipsilateral fore, hindlimb elevate alternatively - viable gate for STB racehorses and some other breeds - considered an impure gait for most "normal" horses. might be a sign of neurological issues.

how is suspensory body/branch desmitis characterised? how does it differ from PSD?

- variable lameness. usually more apparent than proximal suspensory ligament. US: ligament injuries tend to form periligamentar fibrosis - collar of tissue around suspensory branch. - branches need imaging from medial and lateral aspect. focal or generalised lesions, enlargement, bilateral involvement common XRAY: concurrent bony abnormalities (splint bone fractures, fetlock joint. usually heal fine)

what are the tx strategies of of DJD in horses vs small animals?

- weight control +/- exercise modification/physiotherapey - pain reduction + stop inflammatory process (decrease mediator secretion) - chondroprotection ( wishy-washy term). a lot of things that aren't registered as meds but might in vitro slow down cartilage degeneration claim this. no anti-inflammatory effect. - novel tx concepts - salvage procedures very much the same as OA tx. the reality: cannot be fully cured, lacking evidence-based options

what are the effects of applying a shoe?

- weight of shoe increases inertia - alters concussion-dampening mechanism, increasing impact on hoof - elevates hoof from ground, supporting wall - attenuates contraction of wall of heels during late stages of stance phase - INCREASED pressure on FROG: decrease total wall weight bearing, palmar movement of DP

what are the mobility scores for dairy cow lameness?

0) even weight bearing on all 4 feet, flat back. 1) uneven (rhythm/weight bearing), stride shortened, not immediately identifiable. might be splaying legs slightly. wouldn't rush to pick up, but watch. 2) uneven, immediately identifiable, obviously shortened strides. only trim the lame foot. 3) hopping lame. can't walk as fast as a healthy herd. some will get better after trimming, but often need to be kept comfortable

what are the novel treatments/injections for tx of DJD in horses?

1) IL-1 receptor antagonist protein (intra-articular) - key OA inflammatory mediator. stimulates cartilage-degrading enzymes - no controlled large scale studies in horses - could work for non-steroid responsive - autologous conditioned serum contains IRAP from venous blood 2) Tildren: non-nitrogenous biphosphonate - involved in inhibition of bone resorption, anti-inflammatory properties - licensed for horses in europe for distal tarsal OA, navicular disease - unsure of clinical efficacy - clodronic acid (osphos) similar activity, IM injection 3) Polyacrylamide Hydrogel (Arthramid) - synthetic, non-degradable hydrogen, Intra-articular injection - maybe for nonresponsive cases 4) Regenerative Medicine: platelet-rich plasma, mesenchymal stem cells - little evidence base, pro

what is the pathogenesis of small animal Legg Calve Perthes/Avascular Necrosis?

1) Ischaemia of the femoral head leads to necrosis of the head trabeculae (loosened areas) 2) Collapse of the epiphysis during walking (Fragmentation Phase) 3) Secondary thickening 4) Re-vascularisation + new bone formation with malformation of femoral head (Re-ossification phase). remodelling 5) Severe OA

what are the 3 types of salvage surgery? when are they indicated?

1) arthroplasty: joint replacement or excision - indications in end stage diseased joint (OA, avascular necrosis), or non-repairable articular fractures/luxations - excision = femoral head/neck excisions - joint replacements (total hip, could do elbow or knee) 2) arthrodesis: fusion of a joint - end stage diseased joint, non-repairable fractures/luxations - remove cartilage and surgically fuse joint - low motion joints work best: carpus, tarsus, shoulder 3) amputation: carefully check other limbs first

describe the "might work" treatments of OA/

1) botox (intra-articular botulinum toxin A): inhibits pain pathway neurotransmitter release - significant improvements up to 12 weeks 2) paracetamol (pardale/dechra). alternative if GI issues to NSAIDs. 3) Gabapentin: works for neuropathic pain, but no evidence for OA usage 4) Green-Lipped mussel: has GAGs/Omega-3, amino acids, etc. need >2 months for effect 5) disease modifying injectable drugs: - pentosan polysulphage (cartrophen) - polysulfated glycosaminoglycan (adequan) - clinical trials mixed, not unreasonable to try 6) avocado/soybean unsaponifiables (ASUs) - no canine OA studies .Dasuquin. 7) Hyaluronic acid: no canine evidence 8) platelet rich plasma 9) stem cell therapy: adult mesenchymal stem cells which can differentiate into osteoblasts, chondrocytes, adipocytes and help regenerate 10) glucosamine + chondroitin sulfate. mixed evidence, may need 2-3 months 11) cannabidiol (endocannibinoid receptors) - hemp derived.

what are two types of foot imbalances? how do we assess them?

1) broken-back 2) club foot (too upright?) need two angles to assess it: lateromedial and dorsopalmar xrays 2 deviatons are long pastern, short pastern.

what shoes modify hoof support and wt bearing?

1) classical shoe: distances sole, frog, part of bars from ground - reduces wt bearing part of hoof to walls 2) heart bar shoes/onion heel shoes - recruit frog/bars into wt bearing 3) specialty pads: - shock absorbing - protects thin soles against bruising - check tolerance pressure on the frog

what are the 4 main causes of ovine lameness?

1) claw/skin infectious (scald, foot rot, DD, orf, etc) 2) joint infections: foot abscesses, arthritides 3) muscular diseases: WMD, blackleg 4) bone disease: osteodystrophies

what are 3 goals of therapeutic farriery for navicular syndrome? how are they implemented?

1) decrease DDFT tension at breakover/stance phase of stride - rounding surface of toe/rockering toe 2) make breakover smoother - decrease shoe tendencey to descend into substrate: straight bar or egg bar shoe 3) decrease impact vibrations - shock-absorbing pads

what are the three stages of equine laminitis pathogenesis?

1) developmental: contact with trigger (72 hrs) 2) acute: clinical signs are seen (stance, hoof temp, hoof testers, depression on band) 3) resolution or chronic.

what are surgical Tx for degenerative joint disease in horses/small animals?

1) excision arthroplasty (small animal) 2) total joint replacement (Small animal) 3) arthrodesis or facilitated ankylosis (horse) - pastern, distal tarsus, fetlock, carpus - often salvage procedures

what are 2 goals of therapeutic farriery for DJD in the interphalageal joints? how are they implemented?

1) facilitate ease of movement by reducing lever arm at breakover point - roller motion shoe 2) limit concussion associated with impact - padding

what are the causes of septic arthritis? what are the clinical signs?

1) haematogenous (from focus elsewhere - foal umbilicus, intestine) 2) Traumatic (esp horse) - Lacerations, puncture wounds 3) Local spread from adjacent tissue (e.g. abscess) 4) Iatrogenic (often from surgery or intra-articular injections)

what are 3 goals of therapeutic farriery for low/underrun heels? how are they implemented?

1) hoof angle measure at the heel greater than 5 degree lower than toe 2) re-establish correct bony column alignment 3) support heels how to implement is great controversy. - shorten/round doe - support heel - natural balance type shoe...wedge? pads?

what are ways to examine the horse's hoof? how is this limited relative to common sites of lameness?

1) hoof testers: WILL be on OSCES. 2) palpation (local heat, digital pulses, DIP joint effusion, pastern oedema) 3) percussion - if you have an abscess, it might sound different. one foot on the ground. can also percuss for pain. 4) nerve blocks most common sites of lameness are bone and soft tissues inside hoof capsule. inacessible for palaption.

what are the three types of inflammatory arthritis?

1) immune-mediated: most common - erosive (rherumatoid, periosteal proliferative) - nonerosive (idiopathic type I-IV), SLE, drug rx, breed 2) infective - bacterial, borrelial, protozoal, mycoplama, funga, mycobacteria 3) crystal-induced - hydroxyapatite - calcium pyrophosphate (pseudogout) - sodium urate (gout)

what are the 3 types of CCL rupture surgery? what are the pros/cons?

1) intra-articular: oldest one. human knee surgery where a piece of the achilles tendon is locked in. "over the top". AVOID 2) extra-articular: very good results IF done correctly. a band is place around the fabella/tibia. stops instability whilst fibrosis develops - suture always snaps in 2-3 months but allows for fibrosis in the meantime. 3) osteotomy: femoral condyle like a ball rolling down the slope of the tibial plateau. if we flatten the slope, the knee is stable. neutralises tibial thrust but cranial draw is STILL positive. reliable and rapid return to function, but ADVANCED surgery and various techniques. large breeds best outcome. wt bear MORE RAPIDLY 90% get to 90% but OA will progress.

what are 4 goals of therapeutic farriery for laminitis? how are they implemented?

1) move center of pressure away from damaged lamellae: - wedge on side of foot opposite damage 2) redistribute pressure away from lamellae - apply shoe to elevate foot 3) avoid/reduce pressure at the sensitive sole - shoeing/pads 4) facilitate beakover - rolling/rockering toe, squaring toe, or open toe shoe

what are 2 goals of therapeutic farriery for collateral ligament injury? how are they implemented?

1) move center or pressure towards side of affected collateral ligament - increase surface area of ground contact on one side compared with another - increase width branch on affected side 2) ease torque of DIP joint when turning away from affected side - rounding outer rim on opposite branch of shoe

how do we reduce tension on the tendons and ligaments of horses via farriery?

1) raising heels: reduces tension on DDFT but may increase load on SDT/SL 2) wider width toe region: SDFT. sinks less than heels in soft ground - also thinner branches

what are presenting signs of forelimb lameness?

1) stride/step alterations: stort-stepping (limping), radio stance to swing 2) head signs: head nod, "sink on sound", or head bob if bilateral 3) altered limb movement: circumduction, high stepping, claw scuffing 4) altered limb placement: inward or outward rotation

what are causes of over-strain injuries of the equine tendons? how are they diagnosed via history, eval?

1) sudden over-extension - DDFT? 2) Preceding tendon degen during normal athletic behavior with superimposed sudden over-extension - SDFT, SL most common: bowed leg/bowed tendon (SDFT) affecting mid-medacarpal region. fairly predictable. HISTORY: intense period of exercise. signs can be delayed. - clinical exam: lameness (can be temporary or persistent) EVAL: stance and gait - MP joint extension (fetlock): INCREASED if severe SDFT/SL injury, DECREASED if reduced weight bearing/fibrosed (stiff tendon) - elevated toe: DDFT rupture. no ability to keep it's TOE on the ground (bottom image)

what are 4 common conditions leading to DJD?

1) trauma/use - can be acute or repetitive 2) infectious inflammation (septic arthritis) 3) non-infectious inflammation (small animals) 4) developmental disease - dysplasia - angular limb deformity - flexural limb deforming - OCD

what are the 3 types of CCL ruptures? what are 2 common sequelae of rupture?

1) traumatic avulsion: uncommon. 2) traumatic rupture: very uncommon 3) DEGENERATIVE WEAKENING: seen every week. most ruptures are due to a disease process with a complex pathogenesis due to biology and mechanics, theres just a lot going on. we don't really know. different from humans which is traumatic. when it breaks - that leads to osteoarthritis due to unstable stifle joint. 1/3 also have damage to meniscus, and 50% with complete rupture. meniscus 2ary to the unstable knee. remove damaged seption.

what definitely works for treating OA?

1) weight loss - better to be lean - prescription low calorie diets, measure food, only one feeder, alternative treats, increase low-impact exercise 2) salvage: surgical removal of diseased tissue. do not rush. - arthroplasy, arthrodesis, amputation 3) NSAIDS: AA cascade reduces inflammatory mediators at different levels. consider different NSAID if first choice ineffective - side effects not as bad as owners think, worse if excessive dosing, combo w/ steroid, or pre-existing disease - better effects if longer term - 4-6 weeks at label then taper. then B after washout if A doesn't work 4) omega-3 fatty acids: also acts on AA cascade. N-3 ? N-6. only nutraceutical with high level evidence - fish oils 5) amantadine: only Non-NSAID drug proven to work - NMDA antagonist (like ketamine) and reduces central sensitization and direct analgesic effects - renal excretion - can be adjunct or alternative 6) Prostaglandin receptor antagonists (Galliprant): NOT Cox-inhibitor but similar. 7) anti-nerve growth factor antibodies (new, coming soon) - monoclonal antibody ranevetmab. similar to NSAIDS but no side effects 8) home modification

how is ovine footrot scored?

1-4. 1/2: restricted to skin, called OID (scald) 3: under-running, but restricted to POSTERIOR sole 4: under-running involves hard horn of ANTERIOR sole and ABAXIAL wall left: stage two right: stage three

what are the general clinical signs, pathology, and rational tx of subacute/repararative tendonitis?

1wk-6 months. CS: reduction/absence of lameness - resolution of inflammation - tendon still palpably enlarged, soft - signs of re-injury if exercised too early Pathology: - angiogenesis - Fibroplasia (++ fibroblasts, collagen III, small collagen fibrils formed) Rational Tx: - promote fibroplasia - optimise organisation of scar - mobilisation (early, progressive. introduce trotting > 3 months) - regular US monitoring every 2-3 months - increase based on CSA's "biologicals" - scaffolds, GFs, cell therapy (mesenchymal)

what is a chondrosarcoma?

2nd most common primary bone tumour, but rare. diagnostic investigations same as OSA but have a MUCH LOWER metastatic rate. different distribution too (knee, elbow).

EQUINE ACUTE LAMINITIS: what is the prevalence?

3-4% or 8k ponies/year, frequently recurrent. at any one time, 16k ponies with recurrent laminitis.

what is the conservative mgmt/ non-surgical mgmt of hip dysplasia? what is the prognosis?

70% of dogs diagnosed at a young age functionally doing well by 12-15 months. no apparent lameness or only mild changes. joints stabilise by fibrosis. unsure how severity affects this but conservative mgmt should ALWAYS BE FIRST LINE. (young + old) need to do FULLY >3 MONTHS 1) EXERCISE ADJUSTMENT: not complete rest, but regular short exercise, initially on lead. 10 minutes q3-4 daily, increase 5 minutes q weeks. rest at home i.e. no free access to garden, etc. consistent routing. 2) physical therapies: hydrotherapy. non-loaded therapy. - physiotherapy is ok but not really compliant - water treadmill most useful 3) diet: KEEP LEAN/lose wt. prescription low calorie diets can work if used correctly. measure out food, only one dog feeder in house. alternative snacks - carrots, etc. - JOINT SUPPLEMENTS: omega-3 fatty acid supplementation. other stuff not useful 4) ANTI-INFLAMMATORY PAINKILLERS - NSAIDS - treat for 4-6 weeks if possible (wind-down), warn owners of inappetance, vomiting or diarrhoea

what is in the articular cartilage matrix?

75% H20 for viscoelasticity due to the aggrecan 15% fibres of type II collagen attached to HA, aggrecan. aggrecan = chondroitin sulfate + keratan sulfate attached to a central core

proximal metatarsus to stifle

: reciprocal apparatus. need to appy a single splint on the lateral side. wide board or light medal (modified schroeder thomas splint). the ring component suspends the entire limb. used in cattle a lot. continuous pressure on the inside of the thigh. horse - just the outside component.

What is fluoroscopy?

A video X-Ray that provides dynamic and functional information. viewed on a TV monitor. usually in referral centres.

what is the acute vs chronic presentation of post- traumatic osteomyelitis and how should you diagnose?

ACUTE: SA or LA. injury/surgery. systemic signs (pyrexia, WBCC). lameness, acute onset high grade. swelling/pain on palation, +/- draining sinus. poorly. CHRONIC: chronic, low grade, waxing/waning lameness. historic injury/surgery which never really resolves. sinuses discharge, pain on palpation, potential pathological fracture.

what is the surgical treatment of hip dysplasia?

ARTHROPLASTY: remove the diseased tissues - "salvage procedure": 10-12 months old. if NO RESPONSE to conservative therapy. do not need to rush - make sure they are in pain!! 1) Femoral head and neck excision FHNE/Ostectomy - tissues heal, form pseudoarthrosis (false joint) if rehabilitated correctly - analgesics, exericse, physio, etc - good outcomes if manages well. removes painful tissues - any size, particularly good for small dogs and cats - rare complications - not specialist, relatively cheap - straight cut, NO NECK, no spurs. post-op rehabilitation critical. 2) Total hip replacement: BEST OUTCOME - especially medium-large breed, working, young - >20 most common - 10% complication rate - can be severe - specialist surgery, expensive RVC doesn't recommend either of these. they think it should be conservative and then surgery as tx because many of these dogs need total hip replacements anyway.

what are the types of eternal coaptation and when are they used?

BANDAGES: temporary support (should sound ilke a watermelon) - robert jones (cotton wool) - modified robert jones (cast padding) - splinted support bandage - stabilises fracture, reduces pain, reduces further soft tissue damage, prevents/reduces swelling, ongoing damage to broken bones. CASTS: hard material. usually epoxy. - bivalve (most common) - spica splint -schroder-thomas - walking bar

what is the equine laminitis pathophysiology (what is happening in the foot?)

BM hemi-desmosomes fail between two layers of lamellae (dermal and epidermal). pull of DDFT + weight of horse causes pedal pone to sink or rotate towards the sole. leads to separation of dermis from epidermis at lamellae.

define geometric, dynamic, and natural balance (in relation to the hoof)

Balance: shape/function of foot in relation to ground. geometric balance: symmetry of hoof around sagittal solar plane. don't try to change too much of the foot at once. dynamic balance: foot contacting ground in a pattern natural balance: reference point of formula

what is the process of callus tissue formation?

CALLUS tissue: haematoma -- granulation -- connective -- fibrocartilage/cancellous bone -- bone. increasing stiffness, oxygen tension, decreasing strain. similar to endochondral ossification.

what is the most common cause of HL lameness in dogs? which factors predispose to this condition?

CCL disease. any breed. more likely if: - rottweiler, WHWT, goldens, yorkies, staffies - female neutered - increased weight predisposed breeds younger, small breeds older. ALWAYS key differential for hindlimb lameness. nearly HALF dogs will get it on the other side within 1.5 years.

how should your approach a lameness exam?

COMPLETE: client (history) Observe (stance, gait, lameness) Manipulation (capacity to move) Palpation ( structures, abnormalities) depends on tractability. useful to sedate in all cases.

what is the dutch 5-step trim?

CORRECTIVE: 1) create foot angle of 52 degrees 2) create balance b/w claws 3) transfer weight from sole onto wall, toe, heel IF SEE A LESION: 4) remove weight from a painful claw 5) remove loose/sharp horn

how is equine laminitis diagnosed? what are the clinical signs?

CS often enough, +/- radiography, endocrine tests if suspected underlying endocrinopathy. clinical signs: lameness affecting TWO OR MORE limbs. can be one leg, but not often. - characteristic stance (lean on heels, take weight off toes) - increased hoof walk temp, bounding digital pulse (nonspecific, just means foot problem) - pain on hoof tester pressure at region of FROG - palpable depression at coronary band (it means the pedal bone has moved - WORRY - take xrays NOW to see where pedal bone has moved)

what is the common presentation of dogs with IMPA? how would you investigate?

CS: - variable grade lameness, often severe, often shifting - generalised stiffness (often stilted/crouched) - systemic signs: pyrexic, lethargic, inappetent - multiple painful swollen joints (arthralgia) IMPA most common cause of pyrexia of unknown origin. DIAGNOSTICS: - radiography (if non-erosive, then not very exciting). - cytological eval of joint fluid + arthrocentesis. very important - IF PURULENT: C + S, septic - IF STERILE ( and C/S negative): CBC/biochem/urine, US, thoracic rad, echo, further etc

what is the signalment, CS, diagnostics, and tx of achilles rupture? (common calcaneal)

CS: - dropped hock, claw foot. - middle aged/large breed dogs (dobermans, labs) - thickening in the region, swelling - most often avulsion, but can be degeneration, neoplaia,e tc xrays: mediolateral view of right, left hocks - remodelling of new bone over calcaneous - moderate soft tissue swelling over proximal tip of calcaneous tx: - tendon suture+ calcaneotibial screw: locks hock in extension, takes tension off repaired tendon - conservative tx doesn't work - may happen on other limb

what are general signs of acute tendonitis in the horse? (CS, pathology) and how should you treat it?

CS: lameness, pain on palpation, heat, swelling PATHOLOGY: haemorrhage, inflammation (neutrophils, macrophages/monocytes, increased bloodflow, oedema, proteolytic enzymes) Tx: minimise inflammation. PT: ice, compress, MCP joint support, rest MED: short-acting steroids in first 24/48 hrs, systematically or peritendinously. only in acute phase. beware laminitis. NSAIDS. SURGERY: percutaneous tendon splitting using a knife/needles (usually needle), can combine with intra-tendinous medication.

CT vs MRI: what are the differences? how do we describe opacity?

CT is an X-Ray. MRI is magnets - no radiation. on CT, bone is white/hyperattenuating (same as opacity, but it's called attenuation). MRI: bone is dark because not much hydrogen molecules in it. much better for soft tissues. INTENSITY used. white is HYPERINTENSE.

closed vs. open fracture

Closed = skin intact Open = bone protudes through skin grade 1 = skin wound <1 cm, treat as clean grade 2 = >1 cm, soft tissue damage grade 3 = extensive damage

what are the most common causes of cow lameness seen by vets? (5)

DEEP DIGITAL SEPSIS (result of foul, gone untreated): middle image TOE NECROSIS: bacteria in the environment from DDS infect the P3. very hard to get right. INTERDIGITAL HYPERPLASIA: growth in the centre of the picture. pinches, drags on the floor, gets eroded (rubs on concrete), which gets infected, leads to foul, then DDS. leave alone if no problem, cut out if there is a problem. often get really manky so you need to get them to regress before surgery. WALL ULCERS: potentially result of white line disease, which then leads to an abscess which can get up to coronary band. SANDCRACK: not too often. often related to diet. HIP INJURIES: cow slips/falls after calving. TX: OFTEN CULLING, DIGIT AMPUTATION, ETC. LOOK AT THE HERD LEVEL.

how is ovine footrot diagnosed? treated? prevented?

DIAGNOSIS: - rarely cultures are run. - clin assessment: based on inspection of sample. if mild lesions, may require consideration of environment, breed, innate virulence, temporal effects - sample both lame and not-lame feet - think about newly introduced animals: when did they come in? TREAT: - if many lame sheep w/advanced lesions - reduce prevalence, CULL SHEEP. - footrot mgmt: control is priority, reduce incidence. - AB: PARENTERAL (OTC/AMOXY LA). no trimming necessary. 24 hrs of dry conditions essential. high cure rates (70% + in 2-10 days) - TOPICAL: applied after careful trimming and exposure of all infected tissue. VACCINE: can be used therapeutically. some improve after 1st, 55% after second. Footvax. PREVENTION: - BATHING: weekly walk-through + 3 weekly soak. prevention, NOT treatment. hurts a lot with open sores. - ERADICATION: should be achievable because D. nodosus is obligate parasite, dies in 5 days. requires attention to stray sheep, purchased introductions. - TIMING: sell them before autumn. - NO TRIMMING - treat within 3 days onset of disease, cull repeat offenders 2x/year. THE MORE QUICK, THE BETTER.

ESF: indications, pros/cons

ESF: consists of 3 basic units - pins driven into bone and exit the skin - clamps that connect the pins and connecting bar - connecting bar spans the length of the bone - holds bone into place to heal by CALLUS (secondary bone union) pros: quick, relatively easy to apply - relatively cheap, don't need lots of equipment - can do "closed" fixation - no open surgery - similar technique - wide variety of patients - can be adjusted after surgery cons: - pins can loosen - pin tract infection - difficult to apply compression - cannot achieve perfect reduction

how does one deepen the groove in a patellar luxation surgery?

FIRST: might need medial release to get patella back into position (cut ligaments on the medial side). THEN: DEEPEN THE GROOVE 1) trochleoplasty: rasp off cartilage and bone. forms FIBROCARTILAGE - other techniques better. 2) chondroplasty: YOUNG DOGS <6 months old, elevate cartilage flat, remove (rasp, rongeour) underlying bone, replace cartilage BETTER: RECESSIONS 3) wedge recession sulcoplasty: wedge cartilage + bone removed, deepen groove for 50% patella to seat. improved outcome over trocheoplasty 4) block recession sulcoplasty: better results??? but more difficult than wedge. THEN: TIBIAL TUBEROSITY TRANSPOSITION. if tibial crest needs to be further over. the ones that need surgery often need this. if you don't need this - did you really need surgery? CLOSURE: TIGHTEN LATERAL TISSUES.

treatment/prognosis of canine OCD (osteochondrosis)

FLAP: source of pain. - surgical removal recommended, curettage defect. arthrotomy, arthroscopic. minimal OA, excellent long term prognosis if treated young. - flap spontaneously break off: improves comfort, could interfere w/ biceps. - conservative: symptomatic improvement, but removal is better - bigger lesions/presenting when older = WORSE OA

what is sheep lameness causes often confused with?

FMDV. but that would require other symptoms on other part of the body. but it is very subtle and you should be on the lookout.

how do you recognise lameness from the side (Horse)?

Fetlock extension (Fetlock Drop) - usually more pronounced on opposite (sound) forelimb or hindlimb. exception: tendon, suspensory ligament damage changes in limb flight characteristics: - cranial, caudal phase of the stride don't really need to do if it's a pronounced lameness.

what injections are used to treat DJD in horses/dogs?

GLYCOSAMINOGLYCANS ADEQUAN: extract from bovine lung/trachea. mechanism: MMP inhibition, stimulates HA production, matrix synthesis. intra-articular injection: higher concentration, increased risk of sepsis, non-septic inflammation (flare) licensing. recommended dose: 500m IM CARTROPHEN: similar. has a vascular component - pentosan polysulphate. mobilises thrombi, fbrin, lipids, cholesterols. - inhibits platelet aggregation SODIUM HYALURONATE - give stringy-gluey appearance to fluid "viscoelasticity". major structural component of articular cartilage matrix, synovium (synthesized by type B synoviocytes). - anti-inflammatory function (might block way for inflammatory cells). - speculative mechanisms - administration: intra-articular, IV, per OS - degree of polymerisation depends on price. expensive ones are probably better. IL-1 RECEPTOR ANTAGONIST PROTEIN - IL-1 is a key inflammatory mediator in OA which stimulates cartilage-degrading enzymes

predispositions for ununited anconeal process? diagnostics? tx?

GST, basset hounds, american bulldog. mod-severe lameness, elbow pain, effusoin. radiographic diagnosis: straightforward. IF over 20 weeks old - CT: can measure size of fragments. - Arthroscopy: large island of cartilage. can also get coronoid process disease. TX: - conservative: poor - removal: improvement, but longterm OA++ - osteotomy: ∆ pressure in elbow. improve, poss. heal, some OA. - repair/osteotomy: improve, most heal, min OA because less of a ∆ in pressure

recognition of horse forelimb lameness?

HEAD NOD (forelimb): when the opposite (sound) foot lands - elevates when lame forelimb lands - asymmetrical contraction of pectoral mm. (not as obvious) - sound/concussion: harder landing on sound limb -- louder noise.

what is often the history and clinical signs of IMPA?

HISTORY: - onset: acute or chronic - 1-4 affected limbs - inactivity stiffness, usually more severe/longer lasting than OA - travel abroad or UK - exercise - medications/response CLINICAL SIGNS: - stiffness, difficulty rising, shifting lameness - multi-systemic (pyrexia, depression) - palpation + manipulation (+/- sedation) - range of motion, pain, heat, swelling, crepitus CLINICAL EXAM: - 35% lame, 40% joint effusions - Ligamentous laxity - Swollen joints (symmetrical?) +/- painful - Multiple joints affected

what is the history, signalment, and ortho exam for Legg calve Perthes/ Avascular Necrosis?

History: progressive hindlimb lameness - subclinical to severe non-weight bearing lameness Signalment: - Small terriers: yorkies, chihuahuas, schnauzers, poodles - 4 months old Ortho Exam: - Pain on hip extension + abduction, muscle atrophy similar to HD in CS

how does an MRI machine work?

Hydrogen atoms have angular momentum. MRI uses huge magnetic poles to align the body's hydrogen atoms. most of them align in the same direction (parallel). then we emit a radiowave which causes them to flip, then remove the radiowave which flips them BACK. flipping BACK is when they then emit the same radiowave (NMR signals).

what is joint ill in sheep? signalment, aetiology, treatment?

LAMBS 5-10 days old. 1-4 joints, polyarthritis. carpal > hock > fetlock > stifle by s. dysgalactiae or erysipelas rhusiopathiae. factors: - hygiene - colostrum supply - naval dip - runt of a twin (no colostrum, grows less fast) tx: procaine, penicillin.

where is the majority of lameness on cows going to be

LATERAL claw of the hindfoot. they bear weight on the lateral claws. IF it's front foot - MEDIAL claw.

what is the most common form of elbow dysplasia?

MCP disease. Signalment: 5-7 months, most diagnosed 12 months. insidious/chronic lameness. worst post rest or exercise SIGNS: elbow pain +/- radiographic OA. - pain particularly full flexion/extension (flexion + external rotation/supination) NOT OCD. microfractured BONE - OVERLOAD. relates to shape - too small trochlea notch, or short radius.

what are the two luxations of the patella and how do they present?

MEDIAL LUXATION: may have genu vara (bow legged) +/- stifle hyperflexed (image: MEDIAL bow distal FEMUR, COMPENSATORY bow proximal TIBIA) LATERAL luxations: may have genu valga (knock-kneed) +/- stifle hyperflexed. walk dog a few steps and repeat.

what should you look for in diagnostics of OCD on the talus? how should you treat it?

MEDIAL talar ridge flattening, fragmenting - occasionally lateral ridge - effusion - osteoarthritis CT TX: - mild signs: conservative - significant signs: surgical. arthrotomy/arthroscopic removal of fragment, OA progressed, or pantarrsal arthrodesis (fuse all the joints if severely affected) prognosis: NOT SURE. not very much evidence.

how is equine endocrinopathic laminitis prevented?

MINIMISE NSC (only determined by analsysis) - encourage grass to grow, then cut it and take it away. leave the horse with a short length of low carb grass - make hay with grass that is mature crop, post seed - soaking can reduce but not consistent - base diet on forage/fibre, not sugar/starch. if need extra energy: oil, unmollassed beet pulp. - if feed cereals: ensure cooked (easier to digest), smaller meals for lower insulin response - vit/mineral supplement: cinnamon, magnesium, chromium. none of them have any scientific evidence but won't do any harm

what factors influence the decision-making process of amputate/salvation?

NON-TREATABLE injuries: this is few. but loss nerve/blood supply is an absolute indication for amputation. AVAILABLE EXPERTISE: depends on the case CONCURRENT INJURIES FINANCIAL CONSTRAINTS PATIENT FACTORS: a small yorkie could be fine as a hindlimb amputee. active 40kg GSD would have significantly impaired qualityf o flife. OWNER COMMITMENT - lengthy and expensive process, repeated operations, outpatient visits. WELFARE: distressing to patient. COST-BENEFIT ANALYSIS: includes finances, discomfort/distress, risks, owner time, quality of life, best cosmetic appearance.

why are OA and ageing distinct?

OA is NOT a consequence of ageing, it just increases likelihood in combination with genetics, etc.

What is bone spavin and where is it found? how is it treated?

OA of DITJ and TMTJ. osteophytes usually found on inside lower point of hock other dx: distal tarsus fracture, cunean bursitis, soft tissue injury tx: - intra-articular corticosteroids - NSAIDS - Tildren (also used for navicular disease) - Arthrodesis DITJ + TMTJ: surgical (drilling, plates/screws), laser (best outcome), or chemical (alcoho, monoiodoacetate) - cunean tenectomy - neurectomy (tibial nerve) - remedial therapy prognosis: fair to good

what is the most common joint disease in horses? why?

OA. 60% of lameness (53% of racehorses are lame). - elastoviscosity of synovial fluid is abnormally low - give sodium hyaluronan

what are hindlimb problems of the tarsus?

OCD (osteochondritis dessicans) Degeneration (Achilles avulsion degeneration/rupture) Plantar ligament collapse Trauma - fractures/luxations/soft-tissue damage

what is OID in sheep?

SCALD. superficial/mild D. nodosus of SKIN (more severe = footrot). may cause slight lameness. may resolve spontaneously when conditions become dry. starts with INTERDIGITAL SKIN. readily treated w/footbaths. may be called scald by some farmers. necessary predisposing condition of FOOTROT, predisposes to foot ABSCESS, even arthritis.

what is the prevention/therapy for sepsis-associated laminitis? what about supporting limb laminitis?

SEPSIS: - treat underlying cause - anti-endotoxic therapy (flunixin, Phenylbutazone) - digital cryotherapy SUPPORTING LIMB LAMINITIS: -limb cycling important in circulation - controlled exercise or physiotherapy (but this is impossible until lameness resolves) - can try foot support on good leg.

what is the signalment and history of patellar luxation?

SIGNALMENT: - common cause of INTERMITTENT lameness in small dogs - quite young - spaniels, yorkies, poodles, staffies, pomeranians, chihuahua frenchies - OCCASIONALLY large breeds: labs/flat coats - CATS: not clinical often HISTORY: - intermittent non-wt bearing lameness with significant periods of normal - "skipping" lameness - collapse episodes + massage leg back to normal - abnormal gait/holding limb rotated in severe

what ultrasound settings would you use for a small, superficial body part? what about a deeper structure?

SMALL/SUPERFICIAL: high frequency, linear array fits surface well (tendons, ligaments on top image, eyeball side image) DEEPER: low frequency, sector transducer fits small window (ICS for cardiac exam)

what will you find on an orthopaedic exam of a dog with patellar luxation? what should you determine on physical exam?

STANDING: - comfy hips, tarsi ok (no instability) - stifle: alignment of patellar feels ok/abnormal - no tibial thrust/cranial draw - minimal effusion EXAM: - +/- muscle atrophy, joint effusion - palpation to determine alignment: tibial crest, patellar ligament, patella. if you CANT FIND PATELLA: find tibial tuberosity then work up palpating patella ligament, next bony prominence is the patella - work out where patella is at rest. LUXATING THE PATELLA: - lateral recumbency, stifle extended, patella manipulated medially/laterally for laxity - flex + extend stifle with rotation and manipulate patella. - pain on luxation/retropatellar pain. push patella deep into groove. may indicate severity of change/damage, inform surgical decision making CLINICAL PALPATION MOST IMPORTANT DIAGNOSTIC

how is septic arthritis treated in SA vs horses? what is the prognosis?

Small animals: - ABx (Amoxy-clav) then 6 weeks pending culture - no diff. b/w urgical and medical tx, 94% resolve - may need to remove implants Horses: - acute = emergency - eliminate organisms, enzymes, and mediators that cause cartilage destruction - Abx/Through and through lavage/arthroscopy - intra-articular Abx, IV Abx (penicillin, gentamicin), local regional IV delivery, then oral Abx - resample every 48 hours after: - abx? daily dressing changes, rest, physio/hydrotherapy to reduce adhesions, prevent periarticular fibrosis prognosis: - better if PROMPT and AGGRESSIVE Tx for horses (dogs fine) - also intended use, structures involved, and concurrent bone involvement affect prognosis

what is thrush vs. canker? what are they caused by, CS? (equine foot)

THRUSH: infection leading to necrotic processes in frog area. usually limited to lateral and medial sulci of the frog. CANKER: mixed bacterial infection in deeper tissue layers of the entire frog and heel leads to disintegration of the intertubular horn. - WARM, HUMID env. - cheesy white pus, pungent odour, tendency to bleed - TX: generously resect affected tissue. often need to resect entire frog area. both have VARIABLE degrees of lameness.

what are the most common types of osteotomy's for a CCL rupture?

TPLO (tibial plateau levelling osteotomy or totally pointless leg operation): make round cut and rotate proximal segment of tibia. put a plate in while the bone heals. often do very well. TTA: fashionable. straight cut, use patellar tendon to mimic cruciate. stabilise with plate.

what are the UK guidelines for breeding animals that are predisposed to hip dysplasia?

UK: 1 year of age (US OFA 2 year) - less likely to show OA. don't breed if any OA signs. sedation + XRAYs and 9 features scored. lower = better consider parents, grandparents, and sibling scores Breed specific mean score: breed only if score LESS than BMS. affected by euthanasia of dogs pre-screening and owners unwilling to submit if they think will score highly.

LAMENESS IN SHEEP

VAN WINDEN

radiography of equine laminitis: when to do it? what to look for? how to do it and what should be measured?

WHEN: - first presentation if P3 MOVED (depression at coronary band, softening of sole at point of frog) - not improving from tx HOW: can be difficult if painful: stand on blocks or nerve blocks which can be worse (horse walks on them cuz its feet feel better). take machine to horse. RADIOGRAPHY: - lateromedial radiographs of feet. no fancy views. - markers of pedal bone to measure angle of rotation to look for sinking down dorsal wall - MEASURE: dorsal hoof wall (starting at coronary band), +/- point of frog or distance between coronary band and top of pedal bone

what is a keratoma? aetiology, treatment?

a benign growth: columnar thickening of hoof horn extending towards inside of hoof. mostly in dorsal wall. AETIOLOGY: due to pressure on inside structures on the coronary band or sole. this is from mechanical irritation or hoof abscesses. often lyses the distal phalanx with pressure. question: foot abscess due to keratoma or keratome due to foot abscess? unsure. TX: often need removal in standing procedure. cut window into hoof wall and resect, takes one year to grow back out.

what is B-mode imaging?

a cross-sectional, 2-D grayscale US image. most common, used in cardiology, abdomen, etc.

what is a pathological fracture?

a disease in the bone which weakens it, resulting in the fracture. don't do some heroic orthopaedics just for the tumour to keep growing. (image).

what is tenosynovitis? how is it detected?

a dysunction of the tendon sheath, usually SECONDARY to another injury -. important consequences for associated soft tissues and bone. - idiopathic distension causes/concerns: - penetrating injuries - sepsis - non-septic inflammation: primary, often secondary (Annular ligament syndrome, intra-thecal tendon and ligament injury)

what is contagious ovine digital dermatitis?

a new disease. also knowns as super-virulent footfot, severe variant footrot. associated with a SPIROCHAETE infections commence in skin above coronary band of the lateral, anterior, or medial wall of hoof. ULCERS. can underrun, but little exudate/purulent material, no strong smell. less necrotic tissue, no black, liquefying horn tissue. STARTS with ulceration on/near coronary band. extends to hoof wall with underrunning. HIGH morbidity, SEVERE lameness. basically goes OTHER direction of footrot. AUTUMN following wet weather.

what is a PACS system?

a way to store and oragnise radiographic/diagnostic images. you can view them at any computer. Dicom format stores patient info with the image.

what is serosal detail? how can it be lost?

abdominal radiographs. the edge between intestinal loops and fat. not the gas within the gas (that's normal). the serosa is outside and that means that there is a good amount of normal fat surrounding the intestines. LOSE serosal detail with ASCITES. or: puppies. low amount of intra-abdominal fat, lots of brown fat, and small amt of periotneal fluid.

what is the pathogenesis of IMPA?

abnormal B and T cell interaction, maybe a normal response to angtigenic stimulation that doesn't stop (type III hypersensitivity) or a persistent source of antigenic stimulation (endocarditis, neoplasia, etc) - Ag/Ab complex leading to formation of inflammatory products. - host IgG + IgM bind to altered autologous IgG - Ag/Ab complex deposited on synovium - neutrophil/macrophage chemotaxis?

foot bandages for horses

abscesses, surgery on the distal limb (tenoscopy of DFT sheath) - foot is incorporated. due to mechanical irritation, etc, there would be protection/waterproof area.

what is a distal interphalangeal joint flexural deformity? what are the types? signs, tx?

acquired ~ 6 months. usually deep flexor tendon. called "ballerina folds" in adults: forelimbs - chronic lameness - hindlmibs: desmitis of ALDDFT TYPE 1: dorsal hoof wall < vertical TYPE 2: dorsal hoof wall > vertical. theoretically can't correct itself, need to be more aggressive. TX: - NSAIDS (painful) - TYPE 1: exercise, physiotherapy, toe extension shoe. maybe surgery (desmotomy of ALDDFT or DDFT tenotomy) - TYPE 2: SURGERY USUALLY necessary. desmotomy ALDDFT or DDFT tenotomy

what are the four a's of fracture evaluation post fixation?

alignment, apposition, apparatus, activity.

when might you tx a patellar luxation with surgery?

all grade IV/III MILD (II) if also: - pain on manip - retropatellar pressure pain - frequent intermittent lameness: at least weekly - consistent lameness - concurrent orthopaedic conditions operate SOONER rather than LATER

how are infections of the frog/hoof treated? (thrush, canker, WLD)

all similar. - METICULOUS daily hoof care. stall hygiene - DEBRIDEMENT of all necrotic and diseased horn. some places may use maggots for this. - DISINFECT rea - sensitive laminae: BANDAGE - sulci: HARDENING solutions (formalin, iodine, alternatives)

how should one block the DIPJ? what about the navicular bursa?

almost always block DORSAL side of the DIPJ. the palmar is so close to the navicular bursa, u may accidentally block it. BURSA block: hard. aim for the navicular bone in the hoof capsule, 1 cm below the coronary band for the easiest position.

describe the mechanism of US imaging and how to determine the wavelength.

alternating compression and rarefaction lead to a sinusoidal wave. wavelength = peak to peak = velocity/frequency. the image is produced via a pizoelectric crystal that can emit US waves and can also receive them (in the probe).

what is physiotherapy defined as?

an act of veterinary surgery. includes all types of manipulation - oseteopathy, chiropractics. vet ultimately responsible for goals, etc. a good physiotherapist has a lot of knowledge of anatomy, continually palpating/manipulating - powerful allies. does not include acupuncture, aromatherapy. therapeutic basis involves "proprioceptive learning", etc. clients have a very high affinity for physiotherapy but there is often a limited evidence base (difficult to study)

what is coaptation/coaption? what are indications? problems?

an external splint. INDICATIONS - at least partial stability when reduced: minimally displaced fractures, minimal realignment - "internal splinting" - fractures of radius/tibia where ulna/fibula intact, or metacarpals/metatarsals where some in tact - desire to avoid surgery and/or select cheapest alternative - skeletally immature - high/quick healing potential PROBLEMS: - little control, stability to fracture - can result in further malalignment - cannot apply to fractures, proximal to elbow/stifle - can result in serious cast associated injuries (correction can be more expensive than initial surgery) - in most circumstances, surgery provides better stability than external coaptation

What is degenerative joint disease? what is the difference between DJD and OA?

and end-stage of SEVERAL different joint diseases. progressive, inflammatory that results in cartilage degen. very common, incurable, likely to be something many of us will suffer from sooner or later. NOT osteoarthrosis/arthrosis. IF EVIDENCE OF BONE REMODELLING: osteoarthritis. DJD can lead to OA multifactorial. degen of articular cartilage for many reasons - fracture, chip, inflammation -- leading to bony changes which is OA. right: lateral, chip of lateral radius.

distal to proximal metatarsus hindlimb fracture immobilisation (cannon bone fracture?)

angulation at tarsus. proximal tarsus difficult to bandage, splints difficult to apply.

what is foul? (bovine) CS, TX? what is super-foul?

any infection of subcut tissues infovolving fusobacterium necrophorum. can also involve tilomas and treponenes. related to increase in DD. CS: - symmetrical swelling, separation of claws, interdigital skin necrosis yielding a pungent odour. - often assoc w/ FBs, sand in b/w claws. SUPER-FOUL: peracute form, possibly mixed infection. swelling up coronary band. TX: - clean/depride - SYSTEMIC AB for SUPERFOUL (cephalexin, oxytet). Tilosin is too high up the list.

what are shoe extensions? what are they used for?

any part of shoe that extends past normal perimeter. - usually dorsal, palmar, or lateral. - used to change center of pressure and influence motion of the DIP joint. - welded onto outside rim or made that way

what are the types of bars in shoeing? what are they used for (generally)?

any type of shoe that extends from one branch to another. increase area of ground contact on palmar aspect of shoe, shift in center of pressure, and may protect from underlying structures. examples: egg bar, straight-bar, heart bar

what is the inflammatory pathophysiology of DJD?

articular cartilage: failure of homeostasis. cartilage breakdown - matrix metalloproteinases - release of CATABOLIC PROTEINS: IL-1 (used in tx) synovial membrane/synoviocytes releases: PGs, Leukotrienes - neuropeptides - cytokines - MMPs - can be MEASURED in joint fluid Subchondral bone: altered load absorption from cartilage damage, inflammatory mediator release PAIN: present in joint capsule. synovitis, resulting joint distension are painful, exposure of subchondral bone is painful

what is endocrinopathic laminitis? what is the pathogenesis? what are the three conditions it's related to?

associated with EMS (equine metabolic syndrome), PPID (pituitary pars intermedia dysfunction), or glucocorticoids (including iatrogenic, possibly) pathogenesis: prolonged HYPERINSULINAEMIA. not inflammation. NO systemic or GI inflammation. different histological ∆s so you know it's different. MECHANISM: unclear. not ECM degradation, glucose toxicity - possible inappropriate IGF-1R stimulation, leading to endothelial dysfunction. impaired vasorelaxation, and platelet/leucocyte adhesion

how does changing the point of breakover affect the moment arm of the horses's foot? when might this be used?

at the beginning of breakover (the minute the heel leaves the ground), the center of pressure is at the toe. when you move the point of breakover in a PALMAR direction by ROLLING the toe, the length of the moment arm at breakover is REDUCED. however, the breakover duration is increased with a longer toe. USED IN: rocker toe shoe (

what are the "biologicals" as tx for desmitis?

attempt to induce regen rather than repair. 1) scaffolds: AcCell (lyophilised pig bladder submucosa) 2) growth factors: platelet rich plasma (PRP) 3) cell therapy: mesenchymal stem cells - from bone marrow (requires culture) - from fat - alloegnic take bone marrow from sternum of horse. culture it, resuspend in supernatand, and implanted under US guidance. now using for achilles tendinopathy.

how does OCD present/progress in the tarsus? what will you find on history/ortho exam?

background: not seen that commonly. developmental disorder - failure of endochondral ossification - small cartilage flap or a larger osteochondral flap - may be bilateral - medial >>> lateral ridge - osteoarthritis eventually in tarsocrural joint/instability rotties, labs, mastiffs, bull terriers. 5 months - 1 year, older with OA History: stand with upright hock, hindlimb lame ortho exam: tarsal effusions or thickening, +/- reduced flexion, crepitus, pain - pain on flexion and extension, decreased ROM diagnostics: radiographs

how should you deal with FB puncture wounds of the horse's foot? where should you be more worried if it penetrates?

basically an emergency. hoof wall heals well but the structures within them don't. - identify if the nav bone is damaged (contrast in navicular bursa and see if it comes out the nail tract) - remove nail/FB, debride/curretage. lavage if infection. need to SEE what's IN THERE. an inexperienced person might just remove. need MRI to see penetration of nav bone (image - halo), DDFT insertions, tap coffin joint. BACK = SOLAR CUSHION. more worried. FRONT: less worries. debride, palpate, x-ray. if bony structure, the prognosis is good.

differentiate between benign and virulent footrot and what is the reason for the difference.

benign: under-running lesions in few sheep, resolves quickly when treated, clinically indistinguishable from OID (scald). STILL PAINFUL. often doesn't protect from virulent footrot because it's a different serogroup. virulent: severe under-running lesions in a high prop. of infected flock. determined by proteases in d. nodosus.

what are 3 methods for claw surgery on a cow?

best is method 3 - obliquely outwards thru distal P1. so far down you won't affect blood supply thru P1. will get good granulation tissue thru bone. if you go thru P2: disrupt blood supply to small piece of bone, will go necrotic, delay wound healing. thru P1: don't get good granulation tissue unless you completely debride cartilage left in the joint.

what is the correct nail placement of a horse shoe? what direction should it face? what are two types of farriery related problems? what can they cause?

bevel allows the nail to curve outward and go thru the hoof wall. bevel should face inward and be just inside the white line. incorrect placement can cause the the wall to damage/split if too far out and cause lameness/infection/tetanus if too far in. NAIL PRICK: nail driven through sensitive laminae. NAIL BIND: nail driven too CLOSE to sensitive laminae. can cause hoof abscesse,s solar haematomas, foreign bodies.

what's the difference between a navicular fracture and a bipartite navicular bone?

bipartite navicular bone is a congenital abnormality, that may result in chronic low-grade lameness and DIJ osteoarthritis.

other diagnostics for OSA?

bloods, FNA (70% accuracy), biopsy, (jamshidi needle/michele trephine), open or closed. 80-90% accuracy.

what are the 4 categories of non-erosive IMPA?

blue = most severe. I: idiopathic (50%) - early RA? REACTIVE: II: remote infections (endocarditis, urorgenital) - 25% III: GI disease/hepatic IV: neoplasia (<10%)

what is the pathophysiology of hip dysplasia? how does it change over an animals' lifetime?

born normal (genetically predisposed): laxity from 30 days onwards. hip will ricochet around in the cup. increase in synovial fluid, changes in capsule/soft tissue. at birth: normal hips. 1-2 months develops laxity. then hip subluxation leading to either cartilage erosion (polished subchondral bone) +/- acetabular rim microfractures. leads to inflammation/pain, increased joint fluid/capsule thickening, and osteoarthritis. BEGINNING: clinical. then the bone adjusts. then it might become subclinical and then come back in OA.

what is an MP joint flexural deformity? tx?

can be a number of ligaments (fetlock) congenital or acquired (after chronic SDFT tendinopathy in adults) tx: exercise, physiotherapy, toe extension/raisedd heel shoe. - splints/braces (can cause sores) - surgery: cut check ligament or SDFT, whaever is the tightest

what are the criteria for patellar luxation surgery? when might one NOT choose to perform surgery?

can be tricky - not simply grade. make GLOBAL view on clinical impact. may not influence OA progression. consider: - is there a clinical problem? - evidence of pain/OA - 20% complication rate with p. luxation NON-SURGICAL: - incidentally identified low grade (I/II) with no lameness, no discomfort, and happy life - highly infrequent SKIPPING lameness (once a month, etc) may benefit from focal physiotherapy (improve quads mechanism)

what is the d. nodosus vaccine? how does it work/what effects does it have?

can be used therapeutically - some improve after 1st, 55% improve after 2nd. called footfax, covers 10 serotypes. will NOT elim from flock or prevent all cases. 2 doses, 6 wks apart. 12 wks protection afte 2nd dose, may need >1/year, annual booster.

what is dichelobacter nodosus? what is the variation between species and how does that affect CS/Tx?

can only survive in ruminant feet, up to 5 days on pasture. range of strains with varying virulence. 10 antigenicaly distinct categories (serogroups) virulence: influenced by proteases. determines severity of infection. mildest forms cause BENIGN footrot -- INTERMEDIATE -- VIRULENT footrot. most flocks: mixed-serogroup infections.

how does computed radiography work? digital radiographY?

casette stores information as energy which is released as white and saved as a radiographic image, which then becomes a digital imag.e the plate directly converts radiographs into imaging - no processing. allows for nearly RT viewing so that you can re-do them if you need to. plate doesn't have to be taken out.

digital dermatitis: cause, scoring?

cause by Treponemes - infectious. causes red lesions. CLASSIFICATION: - M1: horseshoe cleft lesions <2 cm - M2: >2 cm. red, raw, acute lesions. if you pick it up and poke it, the cow will try to kick you. - M3: regressing. hyperkeratosis. TREATMENT: - acute: topical oxytet, clean, dry. leave uncovered. - M4: clean, debride/debulk (under local as necessary), bandage???? avoid where possible. can also use: copper gel/spray, salicylic acid, tetracycline.

what are the types of DP fractures? what is the aetiology, and how are they treated?

cause: acute onset severe lameness from exercise or kicking out. Type 1: fibrous non-union. not a huge problem. type II/III: arthritis causes. wing, articular. attempt fixation/compression. take MRI/CT if necessary. type IV: insertion of common digital extensor. involves DIP joint. displacement by Common digital extensor tendon. matched fracture bed and fragment. - variable shape of extensor process, and might have 2nd degree ossification centres. - tx: removal via arthroscopy, arthrotomy. type V/VI: communited and solar margin. conservative mgmt. - type V might need a transfixation cast - drill pins thru healing bones. external fix by suspending limb distally. ALL can be painful. treat with BAR SHOE to reinforce the hoof wall to eliminate the hoof mechanism, however it may interfere with bone healing.

what are the cellular and extracellular consequences of cartilage ageing?

cellular: apoptosis, cellular senescense and oxidative stress, and telomere shortening, and DNA damage: lead to gene changes, which lead to protein changes extracellular: accumulation of degredation protein products, and non-functional/fragmented matrix from

what modifications can be made to the cross-sectional profile of the horseshoe?

change width/depth web - increased width = surface area ground force, decrease traction - nonsymmetrical changes - center of pressure moves to thickest side change rims profile: - rounding/rockering of toe - change length moment arm beginning breakover add creases: - increase traction - performance enhancing

how can we use US to examine the bladder?

check prostate/stones on xray. hard to see. sediment in urinary bladder. wall thickness of bladder can be assessed. image: it has irregular lining and hyperplasia - was diagnosed with transitional cell carcinoma.

clinical signs and diagnostics of septic arthritis

clinical signs: - lameness - hot swollen joint - +/- pyrexia - +/- systemic signs (<16% of dogs will die secondary to sepsis/SIRS) diagnostics: - arthrocentesis - C/S - imaging??

clinical signs, pathology, and tx of chronic tendonitis?

clinical signs: - tendon size decreases - tendon less pliable - reduced fetlock extension pathology: - collagen transformation from III to I - x-linking - thicker collagen fibrils rational tx: promote remodelling, prevent re-injury - controlled ascending exericse, lower level - ultrasonographic monitoring surgery: - desmotomy of the accessory ligament of the superficial digital flexor tendon (superior check ligament). ABOVE the carpus to minimise P forces on tendon. rarely used, expensive. - higher incidence of suspensory desmitis - carpal sheath approach

what is the prognosis of equine laminitis? what affects prognosis?

clinical signs: - if sinker (depression all way round coronary band) = 20% survival - evidence of previous attacks - decreased 20% radiographs: - rotation >11.5, significantly reduced - D > 15 mm sinking - 40% chance of returning to soundness. but on the whole, it's very very unpredictable. pasture-associated laminitis: more likely to survive if small, no previous laminitis, ACP tx, low body weight.

guidelines for external coaptation: which fractures, how?

closed, minimally displaced, stable, paired bones, young animals with high healing potential, 50% contact rule. heavy sedation/GA. manipulate leg to improve alignment. repeat radiographs to ensure apposition is adequate. reduction: varies b/w patients. juveniles tolerate greater displacement w/out developing delayed or non-union. open-toe bandage or casts when possible to monitor for swelling. PERFECT reduction often not achieved, but proper joint alignment must be maintained. failure to align major bone fragments can induce rotational/angular malunions, cause functional gait abnormality, or painful lameness from secondary OA.

what types of fractures are external coaptation good for? what forces can it resist?

coapted are stable to bending/rotation. unstable compression/avulsion. suitable for transverse, some simple oblique, paired bones (fibula, ulna intact) unsuitable: not comminuted, usntable spiral, oblique also consider: - location - reduction (?) - age/breed/temperament of animal - finances

what is annular ligament syndrome? how is it detected?

common cause of tenosynovitis (inflammation of tendon sheath). swollen tendon sheath with notch at level of annular ligament. however this is nonspecific, a lot of tenosynovitis can cause this. CS: 1) lameness (mild to moderate) - minimally responsive to rest - occasionally irregular gilding of tendons 2) distended digital sheath 3) "notch" at level of PAL DIAGNOSTICS digital sheath analgesia (usually positive but may not be 100%), mechanical component to lameness US: >2 mm in thickness

anatomy of the elbow

complex hinge + supination/pronation - skeletally immature: open physes. makes it more complicated green: radius yellow: ulna red: medial coronoid process (superimposition of radial head, humerus) other red in back: anconeal process. those make up the ulnar notch, where the humerus sits in. MCP causes the most problems. (A)

why is it so hard to treat OA patients?

complexity in targeting the cytokine cascade - there isn't one target. most strategies are painfully slow in efficacy. anti-inflammatories have high risk factors.

what is compression mode, neutralisation mode, and bridging mode?

compression mode: implant squeezes fracture ends together. primary bone union. neutralisation mode: fracture is reconstructed, implant protects it bridging mode: implant takes full force generated by load

how does cartilage respond to loading, tensile strength, shear force, etc? how does this work?

compressive loading and unloading due to high amount of water, collagen, proteoglygcans aggrecans: hydrophilic due to O-So3 Collagen: tensile strength. resists osmotic swelling and builds resilience. compression: water comes out unloading: water comes back in.

which joints are usually affected by OCD (ostochondrosis) and how does it vary by species?

condition of developing cartilage and supporting bone. - fast growing, high performance patients - dogs: elbow, shoulder stifle tarsus - horses: stifle, tarsus, MCP, POP, DIP - pigs: hip. - broiler chickens: stifle

what are flexural limb deformities?

congenital (possible uterine malpositioning ) or acquired (developmental orthopaedic disease, involved in loading of the limb) tx: conservative. exercise, shoeing. - if FAIL: splints, release of structure.

what is tendon laxity? tx?

congenital or acquired (secondary to casting) Tx: - spontaneous recovery - heel trimming - heel extension show - controlled exercise

how is legg calve perthes/avascular necrosis treated?

conservative INNEFECTIVE. 1) femoral head and neck excision 2) (THR)? send for histology +/-

how should a CCL rupture be treated?

conservative mgmt: - cats/dogs < 15kg - old lit. harder to see when they are lame. SURGICAL TX: - if no response after 8 wks: surgical stabilisation. prof honestly rec's surgery for all of them. - dogs with meniscal injuries DEF do - 30-40% of cases. - stabilise knee joint but doesn't stop progression of OA. inspect meniscus. - MANY different techniques, all with relative advantages/disadvantages.

how to treat limb deformity due to physis damage?

conservative: aim for self-correction under normalised loading - equine: confine to stall, attend to foot balance (shoe/hoof); ensure good nutrition casting surgical treatment during growth (cut if necessary to let grow) definitive correction in adult

direct healing: what is the process? what are the two types?

contact healing: fragments in contact with tiny gap. normally done by artificial compression (plate). - DIRECT migration of osteones (haversian systems) across fracture lines. GAP healing: implant reconstruction. layered bone forms in fracture gap. so osteones can cross fracture gap. both require absolute stability, no movement

how do corticosteroids treat OA?

controversial intra-articular usage (methylpred, triamcinolone). potent anti-inflammatory but mixed evidence. evidence of joint damage due to chondrocyte toxicity, particularly with repeated administration. beware concurrent NSAIDS. never a first line.

INVESTIGATION BOVINE LAMENESS: which type of cattle is most affected?

dairy: on concrete, more intensified. major concern. welfare issue, 5 freedoms, economic importance (can't show heat, etc)

what are hoof wall avulsions? what do they cause?

damage to germinative layer in coronary band. expect permanently disturbed growth. can be purely cosmetic or cause lameness.

what are the confidently treats, considerations, the worth tryings, and the maybes of treating OA? what about what NOT to treat?

definitely: - wt loss - NSAIDS - Omega-3 - Amantadine - Salvage surgery - Anti-NGF/PG agonists if available consider: - exercise, lifestyle changes (hydro, physio) worth trying: - joint supplements (green lipped mussel), cannabidiol, stem cell therapy, platelet rich plasma maybe: - paracetamol, chondroitin/GAGs, avocado, gabapentin, botox, corticosteroids, hyaluronan DON'T: - tramadol

what is density vs contrast?

density ~ exposure contrast ~ range of grey shades in the radiograph. low vs. high contrast depends on what you are trying to assess?

how do you radiographically diagnose elbow dysplasia?

depends on aetiology. can usually diagnose UAP, OCD, incontruity. superimposition makes MCD difficult. OA, UAP, or OCD = strong suspicion, then MCD = elimination. use CT/arthroscopy to confirm.

how are the two lamellae related in the equine foot? how are they attached?

dermal and epidermal lamellae interdigitate. each projection from dermal and epidermal lamellae have secondary lamellae to increase the surface area. BM is anchored via hemi-desmosomes (two layers of lamellae)

what is white line disease (horse)?

deterioation of white line of hoof capsule leads to loss of bond between hoof wall and sole. poor-quality horn gets colonised by diff. bacteria, fungi - WARM, HUMID env (like canker) makes it worse. - often CHRONIC - comes back after several resections

how can exogenous corticosteroids lead to equine laminitiis?

dexamethasone reduces insulin sensitivity, causes exaggerated increase in insulin PL. only RETROSPECTIVE studies - tenuous link b/w iatrogenic steroids and laminitis. pred increases chance of recurrence, not initial event.

diagnostics of osteomyelitis, tx+ outcome. can you prevent it?

diagnostics: - radiographs (only 60% specific), - FNA: cytology in-house (look for neutrophils, ic bacteria. try to be careful b/w septic arthritis and immune-mediated polyarthritis) - Biopsy (infection vs tumour, esp. if chronic) - C+S to tailor Abs or histology. - neoplasia is a big ddx. Tx: prompt. more than just ABs: explantation, local Ab, monitoring. might consider surgical debridement, immobilisation, nad lavage. prognosis: variable but guarded, often recurring prevention: good surgical technique, appropriate periop protocols.

foot abscess of sheep: presenting signs, causative bacteria, aetiology, and predisposing factors, and Tx.

disease of DISTAL INTER-PHALANGEAL joint. severe lameness but low morbidity. BACTERIA: common in environment. F. NECROPHORUM, T. PYOGENES. commences in the IDS with trauma/compromise of skin integrity. ATIOLOGY: - wet, persistent - stones - extends to all underlying structures and joint. FACTORS: - heavy sheep (rams, forefeet or preg. ewes, hindfeet) - OID/footrot TX: - parenteral AB early. - DO NOT: footbathe, attempt drainage. low success rate unless maybe pet sheep. generally too late. might want to amputate toe. - some spontaneously recover, many left permanently lame

what is ovine footrot? what pathogen is involved and what factors predispose?

disease of the interdigital skin, sensitive laminae of the claw. the "second" stage of scald. 40% of lameness is caused by footrot or more. dichelobacter nodosus infection (scald) essential, then produces keratolytic proteases (enzymes) facilitating penetration of F. Necrophorum (abscesses, arthritis). involves SKIN + HORN (OID just skin). SMELLS. influences: climactic, environmental factors. spread unlikely when mean daily temp <10 C. feet must be predisposed by sustained wetting. higher = less waterlogged = less spread. spread in SPRING, SUMMER (moisture) IMAGE: scald/early stage footrot.

what is white line disease? pathogensis, treatment?

diseaseed horn affecting junction bw sole an wall (bruising -- separation/fissure -- abscessation -- ulceration) - last stage (wall ulcer) due to sever, chronic pain - starts with bruising - linked to tight turns - stuff gets stuck in there which makes it worse TREATMENT: CATCH EARLY - drain pus - pare out to allow good drainage: SHARP KNIVES!!!!! - cut away dead horn (can be done 2 wk later) - block onto heallthy claw - NSAIDS esp swlling - AB product (oxytet spray) Prognosis: generally good unless infected with treponemes.

step 3 of foot trimming (bovine)? (after fixing angle, changing depth of both claws)

dish out "model" the ulcer cite. dish WIDER on the lateral claw because that's where most of the ulcers are. this pushes the weight bearing out to the white line which is the strongest part of the claw.

diaphyseal fracture repair: what 3 things do you do to evaluate the fracture?

displacement: how far are the ends apart? - what will it take to get them back together? fragments: can the fracture be reconstructed? stability: will the fracture have any inherent stability if it's realigned? - what forces will act on the fracture when it's loaded? - most bones are curved so they aren't loaded down the central axis, and bend where they bear weight, developing shear forces perpendicular.

what is the aetiology of osteochondrosis?

during development: cartilage becomes bone - requires blood supply for endochondral ossificiation. issues with vasculature in cartilage = doesn't form bone. thickened, avascular plug that goes necrotic. - may cause fissure/flap formation left: flap of cartilage

what are the radiographic signs of an animal with Legg Calve Perthes/Avascular Necrosis? what angle should you use?

earlier: moth eaten/apple core later: flattening/mottling VD (may be clearer on frog-leg) and lateral pelvis.

what is the ultrasound version of opacity? what might cause things to be decreased or increased opacity?

echogenicity. hypoechoic = less opaque. hyperechoic = more opaque. it's a RELATIVE term, not an absolute term. hyperechoic: - fat - glycogen - collagen - vascularity - crystalline material hypoechoic: - oedema

how does elevating the heels affect the balance of the horse? when would you do this?

elevating the heels causes the foot to rotate in the direction of flexion in DIP/PIP joint. this DECREASES TENSION in the DDFT, SHORTENS EXTENSOR moment arm. stance DURATION not affective. USED TO TREAT: affecting one thing might make another thing work. ^ heel height = ^ suspensory ligament but reduct DDFT forces. lots of farriers don't like heel wedges but it's temporary just to help DDFT heal.

review the anatomy of a long bone

epiphysis end physis = growth plate

how do film xrays work?

film - dark room that reduces silver even further so you can see it, then fixes it so it stops changing, and then washes it. there are machines that do that automatically. storage takes up a lot of space and need to be well-identified.

what are the phases of walking in a horse? what is the ground force reaction?

flight phase: hoof is off the ground stance phase: hoof in contact. ground force reaction: impact on the foot. magnitude depends on wt, speed, type of surface. most critical phase of stance phase to develop injuries.

what is an uncomplicated sole ulcer? how is it treated?

full sole-thickness hole which the chorion can prolapse through. PATHOGENESIS": long (months). lateral hind claw is weight bearing, overgrows so all the weight is on it. becomes a bruise which impacts horn growth on the pressure point, which becomes an ulcer. concrete and lack of trimming. the ones in the back of the group wait the longest, more likely to become lame. then they are slow so they are more likely to be in the back. TREATMENT: some say you need to just leave it. if it's big and painful, need to relieve weight/pitching around the ulcer. open it up. so the sole is tapered down around the chorion. THEN: Block on other side + antiinflammatory. can greatly improve outcome. TOPICAL ABs, NSAIDS. nursing and clean yard, no cauterising wound. prognosis: generally OK. recurrence next lactation possible, reduce fertility/lifespan. PREVENT: shorten standing time, TRIM/TREAT EARLY (bruising). biggest risk is prolonged standing + BCS after calving (+/- subacute acidosis) while the suspensory apparatus is weakened and fat pad is reduced.

what are the three main components of cartilage? what is the function?

functions: - bone growth (foetal development) - resists compression - resilience - suppot - flexibility - lubrication/movement at diarthrodial joints components: - ECM of hyaline = collagen Type II - proteoglycans (aggrecan) - water. - smaller amounts of other collagens and proteins necessary for tissue organisation, homeostasis

how are hoof cracks treated?

goals: - identify/manage balance issues - unload injured region - stabilise hoof wall implementation: - appropriate trimming - realign solar margin of P3 parallel to ground - unloading/floating displaced region: properly fit shoe with rim pad, minus the area of the pad that would require affected quarter + heel - double trimming: second trim performed under the proximally displaced quarter/heel - plate, screw wire, polymeric fabric

what is supporting limb laminitis?

good leg at risk of laminitis when supporting lame leg. severity and duration of lameness are risk factors. HIGH mortality. thought to be inadequate perfusion because it's standing the whole time (doesn't load + unload leg)

how does one stage OSA?

gross metastasis (15%), but also micromets which are undetectable. also goes to other parts of the skeleton. QMH: CT the whole dog to look for other bone/lesions, can do scintigraphy but a big bother. PALPATE all bones. if pain - take an xray. ∆ outcome and tx if there are mets/micromets.

what is the aetiopathogenesis of elbow dysplasia?

growth disturbance = asyncrhonous growth -- abnormal loading. radial-ulna incongruity. they grow different proportions from different sides. - SHORT radius = pressure on MEDIAL CORNOID - LONG radius = pressure on ANCONEAL PROCESS trocheal notch dysplasia: humero-ulna conflict

how should you exam a small animal with DJD?

have time for a thorough investigation. radiographic findings correlate poorly with clinical signs. 1) HISTORY: duration, specific event, # of limbs, previous tx, behavioural changes 2) EXAM: wt/BCS - lameness exam: identify, score/10, localise, palpate/manipulate, pain/heat/swelling/crepitus, joint thickening/effusion, reduced ROM - muscular atrophy 4) Synovial Fluid analysis (often nonspecific, rarely done). values not very related 5) Xray/US/MRI/CT. radiographs first. 6) Arthroscopy (assessment of cartilage health, synovial biopsy) image: medial aspect of tibial plateau. meniscus has split, is protruding from wt bearing space. can see more of soft-tissues

what are the screening programs for elbow dysplasia?

high heritability (.7) but polygenetic. Xray screening programs not totally reliable. BVA KC scheme: 3 view elbow radiographs. - >1 year, sedated/GA, etc. - Xrays are graded (0-3)

OCD of the canine shoulder: how to detect? (History, PE, orthopaedic exam, diagnostics)

history: 4-8 months old commmonly, may be older - progressive forelimb lameness, uni or bilateral PE: forelimb lameness. may have muscle atrophy shoulder region. pain on shoulder flexion/extension, not palpation Orthopaedic exam: start normal side, leave shoulder last Diagnostics: radiographs medialateral/cdcr shoulder - obvious lesions - CONTRAST ARTHROGRAM for non-obvious lesion - CT/arthroscopy often not needed. IMAGES: mineralised flap (right side) - lateral view.

how to detect elbow dysplasia? (history, orthopaedic exam)

history: forelimb lameness/head nod - from 5-7 months, most diagnosed 12 months - insidious to chronic lameness - worse post rest or exercise __ - possibly shift sides - frequently BILATERAL - improvement on nsaids orthopaedic exam: - forelimb OUTWARD ROTATION paw, elbow close to body (accomodate pain in elbow) - reduced wt bearing - muscle atrophy - elbow effusion caudal/lateral to lateral condyle

what drives the OA process? how does ageing play a role?

homeostatic imbalance and has a poor regenerative ability. factors: - age: cartilage thins, especially horse stifle joint, regardless of exercise. may or may not be related to DJD. - joint congruency: thickness and congruency are inversely related. need a thicker cartilage to make incongruent joints equalise pressure. - cell depletion and molecular alterations: cellularity decreases, poor response to growth factor and cytokine susceptibility - senescence - proteolytic enzymes - genetics: chondrodystrophic - environmental - mechanical trauma - obesity - larger dogs not classical inflammatory/arthropathy, however it's a chronic disease with low levels of pro-inflammatory cytokines

what are shock-absorbing shoeing? whats the function? what is "shock"?

hoof shock caused by pain, ischaemia, or OA degeneration solution: interposing pads/sole packing between shoe and hoof. - specialty shoes that absorb on ground surface

palpation and hoof testers: how is it used in an equine lameness exam?

hoof testers, SDFT insertion, digital sesamoidean ligaments, digital pulses.

what is the basic lameness principle? how is this affected by therapeutic farriery? what are the goals of therapeutic shoeing?

horse overloads the other feet because he is lame. can cause conformation changes/pathology down the road. aim of therapeutic farriery: to load the foot better on the ground. - moderating concussion - moving the center of pressure

where is hyaline vs fibrocartilage found in the body? what are their differences?

hyaline: articular joints, nasal septum, trachea/larynx. THIN - 10 MM in foal but <1mm in adult fibrocartilage: intervertebral discs, meniscus, ear (elastic).

what are complications of fracture healing/viable non-unions? how to help?

hypertrophic, oligotrophic, dystrophic, necrotic, defect/gap, or atrophic. help: - bone grafting - cancellous (spongy bone) from patient, graft substitutes - cortical grafts for mechanical competence

how to interpret elbow CT for a MCD dysplasia?

idk **** this lecture. arthroscopy for direct visualisation. fluffy cloud on arthroscopy = disease.

what are types of therapeutic exercises?

idk body slings n shit.

tx/outcome form OSA? what does it depend on?

if +ve for mets: palliative tx. - analgesics +/- pamidronate (wks/months). - amputation if NO BONE mets. +/- chemo. 4-6 month survival. removes source of pain. carefully assess for other ortho/neuro dx - radiation +/- chemo, all palliative survival 4-8 months. radiation is good analgesia but can cause pathological fracture and is expensive, not very available if no gross mets: curative intent - amputation + chemo therapy (survival time still only 1 year) - limb-sparing surgery and chemo if you can't amputate the lim. CHEMO: Doxo +/- carboplatin.

how should you run diagnostics for older dogs with hip dysplasia? what can you interpret from radiographs?

if older: will see thickening +/- capital mineralisation, osteophytes/new bone, flattening femoral head "mushroom", flattening acetabulum "dishing". subluxation to completely luxoid. clinically: MINIMAL correlation between radiographic appearance and the degree of lameness or disability. treat the DOG, not the RADIOGRAPH. many with severe OA will have adequate hip function.

what if there is curvature of the dorsal wall when trying to do step 1 of bovine foot trimming?

in case of dorsal wall curvature, estimate 8 cm and make sure yo don't hit the pedal bone.

guidelines for placing a cast: how much to cover, what position?

include joint above and below. cast in a standing position.

gigli wires

incorporate onto the limb - facilitates cast removal. apply handles and can saw off the cast.

how do meniscal tears present in the horse? diagnosis, tx?

increasingly recognised cause of hindlimb lameness in the horse. medial more frequently affected. cranial horn is compressed, minimally mobile. CS: moderate to severe lameness. eval: palpation: FT and FP joint distension, palpate medial meniscus displacement imaging: radiography, ultrasonography, arthroscopy - tears usually horizontal. assess positiong. tx: arthroscopic debridement is tx of choice - mesenchymal stem cells?

when should surgery be performed in the case of immune-mediated polyarthritis? what surgery is done?

indicated for pain mgmt in chronic disease. persistent inflammation may cause joint subluxation options: arthrodesis, excision arthroplasty, total joint replacement

ROM + stretching as physiotherapy

indications: diminishing effects of disuse, immobility. increases flexibility, reduces adhesions/thickening, improves extension. small gains slowly but effectively. difficult in the horse (lateral recumbency). PASSIVE ROM: can do early (before standing) - analgesia/sedation/relaxed animal - limb supported by therapist, joint isolated - single joint flexed util limits reached, or all limbs together. 15-20 2-4x/day. also helps improve proprioception: need a proper "cycle" of motion: the only "good" movement is "real" movement. want the patient to use the limb in a constructive fashion. whole range of motion (abduction, flexion, exxtension) ACTIVE ASSISTED ROM: ACTIVE ROM: if walking/trotting. chance exercise - walking in water, different surfaces (sand, vegetation, rails, tunnels, etc)

what is direct vs. indirect healing?

indirect healing: normal process. forms a bony scaffold at the fracture called a callus that is subsequently remodelled. requires favourable mechanical conditions. - will occur with any gap over 1 mm - tolerate some movement - stronger, faster than direct union - incompletely reconstructed fractures, casts, ESF, no intervention direct healing: direct union of bony cortices with little callus. requires very specific mechanical conditions. speed also depends on age

what is the pathogensis of hoof abcesses in the equien foot? CS, TX? what is a chronic foot abcess? what is quittor?

infectious of sensitive laminae by bacteria. various clinical signs, can happen in shod and unshod horses. can be from nail bind/prick, small rocks, any FBS, or any solar bruising. the draining ones will have less clinical signs. you can localise via hoof testers, digital pulses. chronic ones burst at coronary band - "gravel" is common. QUITTOR: infection of collateral cartilage. is painful and forms fistulous tracts, which requires resection of affected cartilage. often warrants diagnostic iamagine. TX: debride area, drain pus to relieve pressure. no ABS.

adipose neoplasms: what are the main ones you can find in the muscle?

infiltrative lipoma. recurring. radical excision but often recur. liposarcoma is metastasis consider like a soft-tissue sarcoma but fat on FNA, which can lead to misdiagnosis. benign lipomas: intramuscular.

what is osteomyelitis? what are the types? what are they usually a result of?

inflammation of bone + bone marrow, usually due to infection (bacterial) POST-TRAUMATIC: acute, subacute, chronic. - can be from implants which leave a biofilm that can cause infection. - often nosocomial origin, MDRI. cell division is really slowed so antibiotics often don't work. also change pH HAEMATOGENOUS: super rare, young animals. deficiencies of BM + capillaries make it prediliction + microtrauma (like a kick)

which anti-inflammatories are used to treat equine DJD? what are some side effects?

intra-articular corticosteroids can be more potent because they involve arachidonic pathways further up and MMPs. however NSAIDs more common. can be inexpensive, efficient. horses can get protein-losing enteropathies (right dorsal colitis), might have negative influence on cartilage and bone mechanism, +/- GI ulceration and nephritis. COMMON NSAIDS: - bute - suxibuzone (activated into same thing basically - meloxicam - flunixin COMMON STEROIDS: - betamethasone - triamcinolone acetonide - flumethasone - isoflupredone - methylprednisolone acetate

intracapsular vs. extra-capsular non-articular fractures: how to treat

intracapsular: some can be fixated simply due to helpful force distributions - ingress of synovial fluid to the fracture line can be a complication - hips: also complicated by poor vasculature extra-capsular: may be fixated with simple implants as the forces acting on the epiphysis tend to promote stability, not disruptive.

interlocking nail uses, pros/cons

intramedullary device: fenestrated to allow screws to lock the implant to the bone - placed in a jig system, often using minimally invasive technique - used for people advantages: can be used semi-closed - very strong (esp vs bending) for simple, comminuted fractures cons: - requires specialist equipment - implants must "match" bone (tibia/femur) - not commonly used in UK

what is upward fixation of the patella? how can it be treated with farriery?

is a condition in the medial patellar ligament remains hooked over the medial trochlear ridge of the femur making it difficult or impossible for the animal to flex the affected limb. goals: - limit extension of stifle joint by raising heels - encourage hoof rotation by trimming inside wall - better medial breakover by rounding medial aspect of the shoe (lateral heel edge?)

DDFT tears: CS, diagnostics, prognosis?

it leads to navicular system. can image on MRI (top) or navicular bursoscopy (bottom) bursoscopy: explore via DDFT sheath if no obvious xray. ends up in bursa. a flap of protruding granulation tissue is a sign of the tear - resect and give time. this flat causes pain, adhesions. prognosis: only 60% regain full ability. often becomes lame on the other leg. PLANK TEST: accentuates DDFT strain, compresses palmar structures. stim test. hurts. majority: x-ray inconclusive, MRI best.

why is it so important to keep the leg straight, extended when taking radiographs trying to diagnose hip dysplasia?

it's impossible to accurately tell how much femoral coverage there is. make sure the pelvis is not rotated.

describe the horses MP joint.

it's permanently extended. the weight-bearing tendons are on the PALMAR aspect. intra/extra synovial portions of flexor tendons - different consequences, injuries, and treatments (intra vs. extrathecal injuries) flexor tendons have a tendon sheath within a synovial environment. part of

What is the function of the hoof capsule? what is its anatomy? what's the difference between the white zone and the white line? where are nails driven into?

it's rigid and protective but flexible. things get painful in there (stones, etc) because there is no room, therefore no possibility for internal swelling and drainage. WHITE LINE: WEAK point BETWEEN the white zone/zolar horn and the hoof wall (stratum medium). The WHITE ZONE is INSIDE the laminar stratum. hoof NAILS are driven through the STRATUM INTERUM (in between lamellae and hoof wall, just inside the white line.

how do you PE a lame cow that's not in the foot?

just like a dog. rule out foot lameness. - check symmetry, anatomical landmarks like trochanter - feel for heat - manipulate + palpate, feel for crepitus. reaction often SUBTLE. - check fields of cutaneous sensation with 18G needle - manipulate rectal exam.

what is equine metabolic syndrome? how does it lead to laminitis?

key feature: Insulin dysfunction - hyperinsulinaemia, - excess insulin response to carbs - or tissue insulin resistance) - increased fasting [TG], altered adipokines, obesity

what is proprioceptive training? what is an easy first exercise?

key to physiotherapy. movement that the patient makes in recovery, needs to relate to real life. needs to re-learn how to use its limbs correctly. just shifting weight r-l by leaning forces animal to think about where its limbs are. small poles that the animal has to walk over, etc.

what is the role of the CCL?

knee stability: prevents "craniotibial translation" and internal rotation. prevents the BALL of the femur from SLIPPING off the tibia.

presentation of osteosarcomas? CS + PE, diagnosis (key things to look for )

lamenness: chronic, progressive. incomplete, +/- resp from NSAIDS. swelling, acute deterioriation. PE: swelling, bone pain, +/- crepitus, +/- palpably soft cortex. check local LN, full ortho exam, general exam. DIAGNOSTICS: imaging - XRays. CT most sensitive. osteolysis (cortex thins and whittles away), osteoproliferation, periosteal reaction, monostotic (ONE bone. RARELY crosses the joint). no distinct border b/w normal and abnormal.

briefly summarise how farriery can help treat laminitis, navicular syndrome, collateral ligament injury, DJD of the IJ, or susp. ligament injury.

laminitis: rolling/rockering of toe, squaring toe, setting shoe back, open toe shoe navicular syndrome: straight bar/egg bar shoe, absorbing pads collateral ligament: increase width of branch affected side, rounding outer rim opposite branch DJD interphalangeal joint: roller motion shoe (breakover on all side + wedge), pads susp. ligament: wider width toe region, thinner branches

what do you find at history for a dog with hip dysplasia? what about physical exam? ortho exam?

large breed dogs. commonly young (6-7 months). owners note - bunny hopping - problems rising - hindlimb lameness - won't exercise as much - clinking, clunking noises older dogs: slowing, lame, won't jump, difficulty rising. flare-ups. STANDING EXAM: musculature + stance, feet with digits, tarsus, tibia, stifle, femur, hop, and spinal + tail lift to rule out lumbosacral disease. ORTHO EXAM: - PAIN ON HIP EXTENSION/abduction. most important. extend in a straight line relative to the spine if you can - get the animal relaxed. a painful dog may not allow you to do that. - clunking, muscle atrophy if young: unlikely cruciate rupture if older: make sure it's not cruciate

what are horseshoe pads used for? what are they?

layer of leather/synthetic material between shoe and hoof. flat or wedge, complete or partial. uses: - prevent sole from coming in direct contact with ground - provide damping of impact vibrations - change ground surface distribution of forces - change center of pressure - can lead to thrush formation

why didn't antarctic sled dogs have hip dysplasia but they had OA?

leaning/pulling against sled weight was preventing it. they were getting OA from age. high prevalence of hip dysplasia + OA in UK

what are osseus cyst-like lesions? what do they cause? tx?

lesions often found on the DP (P3) near collatearl ligament. vary in significance - use nerve blocks as guidance. benevolent neglect if incidental (seen on MRI). not uncommon, can also be found in nav bone/ middle phalanx. could possibly debride, forage, enucleate if causing issues.

what is the prognosis of elbow dysplasia?

life-long disease process. - OA progresses. may have flare ups. - ends up as OA mgmt, may have many good years of function (elbow joint replacement, alter loading in elbow joint, etc)

immbilisation from sifle to coxofemoral joint:

limb remains controllable due to distal muscle insertions. but impossible to stabilise via external means.

what are the three probes that are used for US? when are they used?

linear: face of the transducer is a straight line. gives you a rectangular image. wider face. good for superficial structures. sector: gives a pie-shaped image, top is a dot and sweeps out. used for cardiac mostly. curvilinear: top is curved too. used for smaller body parts in the abdomen. most general so it is probably the most common. sector or curvilinear useful for looking between structures, like ribs.

how would you do a lameness exam for DJD for large animals?

local analgesia (horses): intra-articular more specific than peripheral nerve blocks. can block navicular bursa. limitations in distal limb. blocks in coffin joint =/ coffin joint problem.

what forces act on the DIP joint during the standing phase?

looking at distal-interphalangeal joint, navicular jointt. DDFT pulls on P3. extensor moment: depends on ground rxn (G) and extensor momen arm (a). flexor moment depends on and flexor moment arm (B), and tension on flexor tendon (T). therefore (G x a) = (b x T)

what is PPID? how can it lead to equine laminitis?

loss of dopaminigernic inhibition -- excessive production of pituitary hormones. the role includes antagonising insulin (cortisol, CLIP) this leads to hyperinsulinaemia -- laminitis.

step 1 of foot trimming: what is it?

measure from coronary band 8 cm down to tip of the toe. make the cut so that the dorsal wall length is 8 cm. if length already correct: move to step 2. if heifer, shorter. THEN, correct sole depth, spare heel. leave extra toe thickness if curved toe. sole becomes very thick at the front of the foot and leaves it up, leaving the weight down through the heel. if she's weight-bearing through the heel and it's overgrown, you will get SOLAR ULCERS in the back of the foot. aim is to correct the angle to ROCK HER BACK onto her toes and not her heels so that the weight is across the whole sole. area cut is a triangle, most part cut is the toe. start on the NORMAL claw: medial on hindfoot, lateral on front foot. get it right and then you can make a template. you can also put a block on this one if you need. WHITE LINE will start to reappear on the foot. slight step of 5-7 mm. keep checking sole to make sure it doesn't go thin. if you start to feel give on thumb pressure - stop. too close to the chorion. measure several times, because over-trimming is an issue.

what are the menisci of the knee? what is their anatomy (attachments) and function? which meniscus is usually affected by CCL ruptures?

medial and lateral. triangular with cranial and caudal poles. MEDIAL meniscus: attached to tibia by caudal meniscotibial lig and medial collateral ligament. important because ad the tibia slides, the medial meniscus gets chewed up because it's attached to the femur. LATERAL: attached to femur. function: improved congruency - load bearing/shock absorbing - collagen fibre arrangement converts compression into tension the blood supply is on the outer rim so it heals poorly but it has good nervous innervation so it's PAINFUL

what are specific therapies for intra-thecal tendon/ligament tears?

medication: HA/corticosteroids. avoid steroids if you can help it. - intrasynovial location = POOR HEALING - tenoscopy/arthroscopy. Manica Flexoria: Remove it completely. good prognosis DDFT: debride. poor prognosis (20-40%)

what can you visualise on a radiograph of a patellar luxation? what x-rays should you take?

mediolateral and caudocranial stifle radiographs: straight stifle = fabellae equally bisected by femoral condyles. don't rely on patella. STIFLE may be NORMAL: clinical palpation is most important diagnostic if HIGH grade: include entire limb. document luxation and extent of bony deformities - OA, stifle effusions usually mild, or other problems (concurrent CCL?)

what is cat "lung-digit"? prognosis?

met of pulmonary mass to digit. present for lameness. poor px: 2 months no matter what.

plating: indications, pros, cons

metal plates attached to either side of fracture site with bone screws. can be used to generate primary or secondary bone union. pros: - compression, neutralisation, or bridging mode - can achieve perfect reduction - no bulky external element - massive range of implants available - minimally invasive and "internal ESF" devels cons: - large equipment range required - large skill base required - normally needs open surgery

what is plantar collapse?

middle aged dogs, collies, progressive HL lameness (degenerative disease of tendons) foot looks like a banana. radiographs + manipulation arthrodesis only real treatment.

lower limb casting in horses

minimal orthopaedic padding - apply cotton stockinet, fix cast felt to proximal margin. less padding = less slipping, less sores.

what amount of reduction is suitable for external coaptation of a fracture? what breed of age?

minimally displaced - 50% rule. at least 50% of fracture ends should overlap on both orthogonal radiographs. SHOULD be more. BREED: juvenile - heal rapidly, well UNSUITABLE: for obese, chondrodysgrophic (can't bandage) or sighthounds (high risk skin wounds) or - distal RADIUS + ULNA in handbag dogs. problems healing).

what are traumatic, fatigue, and pathological fracture classifications?

most due to trauma. occasionally the fractures because of weakening the bone: - fatigue/stress = repetitive high loads causing microdamage pathological fractures: - local weakening of bone (tumour or infection), generalised weakening (hyperparathyroidism)

intraarticular corticosteroids in horses: how are they used and what might be side effects?

most potent. affects cells, humoral medioators. inhibits PGS, IL-1, TNF-a, enzymes (inhibit cartilage-degrading enzymes like matrix metalloproteinases) HOWEVER: - can can cause LAMINITIS - cartilage metabolism/healing: data is controversial. degreased PG synthesis, alteration collagen synthesis. drug choice and volume: bethamesasone, flumethasone, isoflupredone. safety limits.

OSA in cats: differences?

much LOWER met rate.

what factors involve in OCD in the shoulder?

multifactorial. hereditary, calories, calcium, ad lib feeding

how do muscles change adjacent to bone fractures?

muscles acting on broken bone: do different actions. - proximal radius - rather than bring fwd/backward, the bring it outward. that can cause the fracture to become open, decreasing prognosis. might feel moist spot/regional swelling - passive action structures (stay apparatus): suspensory, reciprocal. if that bony column is disrupted, you will get outward motion. need to palpate INSIDE TIBIA on lameness.

what is a suitable location for external coaptation?

need to immobilise the joint above and below the fracture; therefore anything distal to elbow and stifle. would have to cast the whole top end of a dog if it's the humerus or scapula. unsuitable: - articular (need to be put back together perfectly) - growth plate (need to be correctly reduced or the leg will grow abnormally) - above elbow/stifle - do cage rest first. bandaging could make it worse because it makes a massive pendulum by making a weight

complications of external coaptation?

non-unions: toy breed distal radius/ulna. - DON'T cast them. bone can whittle away/disappear. soft tissue complications: - tell owners to monitor carefully. sighthounds more likely to develop soft-tissue injury. 2/3 will develop injury but most very mild. malunions: length discrepancies, etc. from casting in the wrong position. swelling: don't wrap the toes over, only to the tips of the claws. use sequential layers. be vigilant. advice: - daily check by owners: weight bearing, smells, swelling (toes), colour, discharge. - weekly check at vet. - keep covered when going outdoors (plastic bag)

what is thermotherapy? when is it used?

not as frequent - not good for swelling/pain. once INITIAL swelling is decreased, it can help.

how well does tramadol treat OA in dogs?

not at all - fake news. don't give

what joint supplements are given to horses/dogs for DJD?

not regulated. matrix glycosaminoglycans: - glucosamine - chondroitin sulphate green-lipped mussel extract - anti-inflammatory, high in chondroitin sulfate, fatty amino acits, minerals, vitamins MSM (derivative of DMSO) - sulphur source for collagen, matrix metabolism - No efficacy data Devil's Claw - reports, no scientific evidence. - iridoid glycosides that decrease inflammatory mediators. used in traditional african medicine.

what are the rongten signs? what can they indicate?

number, position, size, shape, opacity, and margination. size: change in size alone suggests uniform affectation of organ (hypertrophy, infiltration, etc). - example: hepatomegaly: end-stage cirrhosis, diabetes, HAC, or small because PSS shape: focal/multifocal lesions. nodules, masses (bulges), scarring (dimples), chamber changes, fracture/malunion. cardiac silhouette very difficult to assess. left lateral recumbency can elevate heart apex. also changes across breeds (brachycephalic dogs) opacity: soft tissue not easily distinguished (blood, urine, bile, exudate, muscle, parenchymal organ). radiolucent = fat, air. radiopaque = metal, bone. FAT =/ SOFT TISSUE. greatly affected by thickness as well. margination: edges. periosteal reactions, fluids, infiltrating lesions, adhesions.

what is equine flexural limb deformity? what are the goals for therapeutic farriery and how are they implemented?

occurs in sagittal plane and primarily affects soft tissues. goals: - ability to bear weight on sole - maintain hoof sole on ground - increase tensile forces on DDFT - protect toe implementation: - if digital hyperextension: shortening of toe, glue on shoe with palmar/plantar extension which ∆ at 10 day intervals - if flexural deformity: dorsal hoof wall/toe extension - if box foot: heels should be rasped back gradually, toe extension

what are intra-thecal tendon tears? where are they? how do you detect them?

often in DDFT (forelimbs), - manica flexoria (hindlimb), just above fetlock. loop of Superficial that wraps around the deep flexor tendon. US diagnosis difficult. - lateral or medial echogenic (material) via oblique views. - Manica flexoria instability in longitudinal view. can use CONTRAST tenography.

what is cerclage wire? when is it used?

only used in completely reconstructible fractures. paired wires are twisted tight to stabilise LONG OBLIQUE fractures. must be tight.

when should you shoe a horse? how should you trim/shape it?

only when necessary (wear/tear more than hoof can bear) or part of tx, or traction. trim: flared and sheared heel should be corrected. should be short and proportioned. shape: - should be shaped to food and nails correspond to white line - should cover ground surface of the hoof wall and small amt adjacent sole - extend 2-3 mm abaxially when approaching heels to accommodate expansion of foot - extend 3-4 mm caudally to anticipate fwd movement respect shoeing intervals!

what are the most common grading schemes for SA lameness?

out of 5 or 10. 0 = normal 3 = obvious lameness, both gaits 5 = non-weight bearing

what is NSC? how does it vary? what equine syndrome is it clinically relevant in?

overconsumption NSC leads to endocrinopathic laminitis (fructan + starch + sugar) - NSC = energy from growth of plants. fluctuates widely in pasture, decreases when plant is growing and increase during photosynthesizing - also depends on season, grass - haylage: low, palatable horses can eat their entire daily requirement in 3 hours

what can affect prognosis of limb amputation? what is limb-sparing surgery (endoprosthesis?)

owner's attitude, lol. not BCS, forelimb/hindlimb, anything like that. 88% satisfaction rate after 4 weeks. limb-sparing surgery in case the owner can't amputate. tumour is removed and replaced with plate/stainless steel implant. HIGH infection rate, but 70% excellent use of leg post-op. you can also use prosthesis for the distal limb or stump socket prosthesis.

what are the palpation tests for dogs with hip dysplasia? what are other investigations?

palpation on immature dogs - test hip laxity bardens test: hip lift. >.5 cm abnormal ortolani test: put dog on its side, push down pushes hip out of joint. then as you externally rotate, you feel it back into joint. feeling the click is a positive sign. other investigatons: quantified measures of subluxation: nordberg angle, PennHip Distraction index, and % femoral head coverage

palpation vs. manipulation: function, how to?

palpation: look for pain, change in structure manipulation: moving joint in controlled fashion to determine range of movement, pain related to movement, specific structures in limb

what are the 4 grades of patellar luxation and how does it affect tx/prognosis?

patella IN: - 1 returns automatically. incidental finding, minimal problem, infrequent/no observed clinical signs - 2 stays out once pushed. intermittent "skipping" - observes spontaneously and resolves spontaneously. patella OUT: - 3 can be returned to groove. persistently abnormal stifle function - cannot flex normally. can have subtle lameness. - 4 CANNOT be returned to groove. typically debilitating, crouched stance and gait

what are the two type of equine angular limb deformity? how can you help with therapeutic farriery? what are possible AE with farriery?

pathophys: conformational deviation of limb in frontal plane. - lateral = valgus - medial = varus goals: - balancing forces onto force plates - increase wt bearing surface of foot implementation: - regular trimming every 2-4 weeks - valgus: outside hoof wall is lowered and extensions medial side - varus: inside hoof wall is lowered and extensions lateral side farriery can result in fulcrum effect and P3 fracture, aseptic pedal bone lysis, and hoof abscess

what are 2 goals of therapeutic farriery for pedal osteitis? how are they implemented?

pedal osteitis = demineralization of lower edge of pedal bone (P3) due to inflammation. similar to navicular disease. 1) limit contact with outer sole margins with shoe and/or ground - seating out hoof surface of shoe 2) decrease impact vibrations at beginning stance phase of stride - full pads

how do you recognise hindlimb lameness in the horse?

pelvic hike/drop: pelvic HIKES when lame limb is weight bearing, drops when opposite limb lands drifting: horse moves towards sound limb. lame limbs tracks under body or is posted

what is a physeal fracture? what is a stable vs. unstable fracture?

physeal: happens in skeletally immature animals. physis is the growth plate of the long bone. young animals. stable: after reduction, bones remain in place without force. resists compression unstable: fragments don't interlock - collapse once retaining force withdrawn. don't resist compression.

what three implant systems can resist all the forces acting on diaphyseal fractureS? how are they augmented?

plates/screws external skeletal fixator interlocking nail augmented by: lag/positional screws, intra-medullary pins, orthopaedic wire. not to be used alone.

how can foot puncture wounds be treated with farriery?

postoperative protection of foot after surgery: medication plate shoe, daily wound are by removing plate

joint tumours in dogs - how do they present, diagnose, treat?

present with lameness, +/- joint swelling, large breed, older dogs. issues with dx because they resemble other orthopaedic issues. chronic inflammation might have role to play. FNA/Joint fluid often nonspecific, vague. might not fit. - biopsy + IHC progressive sarcomas. rest +/- pain relief doesn't work. treatment often amputation.

what is a cast made of? what are the layers?

primary layer: cover + protect skin, absorb discharge. melonin, allevyn. secondary layer: absorption, support, pressure. keeps primary in place. - cotton wool (difficult to remove) - cast padding (less bulky, conforms better) - conforming gauze is wrapped over "padding layer" tertiary layer: - vet wrap. holds inner layers together, fixes to bandaged part. barrier against physical abrasion. - casting tape: applied over light secondary layer. how you set casts. forms the HARD outside cast. dunk in water and then gets hard. +/- stirrups

what is an osteosarcoma? where is it most common? which breed/age, etc?

primary tumour of bone. common, older, large breeds. appendicular skeleton (large bones) more likely. towards knee, away from elbow more common. 15% pulm. mets. rottweilers, great danes, greyhounds. bimodal distribution (rottweilers) including young dogs.

what are 2 specific therapies for proximal suspensory desmitis?

problematic disease in the hindleg, can involve the bone. extracorporeal shockwave therapy: high energy sent on bone to disrupt interface b/w soft tissue and bone. - forelimb PSD; 53% at 6 months for chronic cases - hindlig: 41% at 6 months for chronic fasciotomy/neurectomy: only if fail. there are concerns. - hindling PSD which fail to improve after 2 tx

STRETCHING

pushing joint past normal ROM. designed to oppose shortening of tissues, break down fibrosis, adhesion. largely in form of static stretching in animals - can't tell them to stretch.

what is the classic diagnosis of RA? how often is it used in animals?

rarely aplicable in animals. must have 7 of the following, including two of 7,8 or 10 1. Stiffness after rest 2. Pain 3. Swelling of one joint 4. Swelling of another jointrecently (<3m)5. Symmetric joint swelling 6. Subcutaneous nodules 7. Radiographic erosion 8. RF +ve serology 9. Abnormal synovial fluid 10. Synovial histology 11. Nodule histology

hindlimb from coronary band to distal metatarsus

reciprocal apparatus need to be considered . angled kimzey - on toes like forelimb. also under debate. some immobilise in wt-bearing position "ski boot monkey splint". if only bandage material/board splint - can't do that.

what is hydrotherapy used for?

reduces gravity and therefore reduces impact loads, spreads across all joints of the limbs. animals work harder in the water than on land, higher metabolic land. underwater treadmill is the best one. the animal is only partially supported. make sure gait cycle is proper (person in water), flotation jackets, limb floats, etc.

step 4 of foot trimming (bovine)?

relieve weight off painful claw: trim back 2/3 of painful claw or apply block to healthy claw. block is about 2 cm thick and glued onto normal claw, so the diseased claw can heal. can use plastic or rubber.

step 5 of foot trimming (bovine)?

remove loose/under-run horn, hard ridges. in most cases only back 1/3 of inner hind claw should be tidied, back 2/3 of outer hind claw. do this in case of SLURRY HEEL to prevent slurry to move up, force its way between layers of horn.

transfixation casting indications?

repaired or conservatively tx distal limb fracture that is usntable under axial loading fetlock breakdown injuries avoid wtbearing laminitis. need the animal roughly equal wt bearing on contralateral limbs.

muscle neoplasms: what are the two main ones?

rhabdomyosarcoma (rare), haemangiosarcomas can be in the muscle.

scoring and treatment of ovine DD?

score two: top of the horn/interdigital skin. score 5: at the tip of the tow all the way don. antibiotic foot-bathing is OFF-LICENSE. DO NOT DO IT : lincomysin, tylosin topical antibiotic, parenteral AB.

what will you find on radiographs of a younger dog with HD? how should you take them?

sedated/anaesthetised. VD EXTENDED leg and lateral pelvis. straight important - femur. need to fit fabellae in there. in some very difficult to extend the hip fully - frog legs. if YOUNG: look for acetabular coverage of the femoral head. want it to be >50%. can also sea flattening of the femoral head. early 2ary changes can happen as well. beware insertion capital ligament.

what is the function of the patella? what is a patellar luxation? what is the pathophys?

sesamoid bone that redirects forces from the quadriceps like a pulley. the trochlea is the pulley hole. alignment is key. PATELLAR LUXATION: abnormal tracking of the patella. - usually medial in all sizes of patients, can be lateral in any size of patient. PATHOPHYS: 1) problem with devel. of quadriceps mechanim - possibly due to hip/femoral neck 2) uneven pressure on physes: alteration groth dynamics 3) bony deformation: lateral bow of the distal stiful, compensatory deviation of the tibia, and skeletal torsion/angular deformities varying severity 1-4, increasing in left to right in amount of torsion. for the groove to develop, the patella has to be sitting in it. otherwise, it becomes totally flat (grade 4)

simple, trasnverse, oblique fracture: what's the difference? what about comminuted vs. segmental?

simple: 1 fracture line transverse: fracture angle <30 perpendicular to long axis of bone. - interdigitating = irregular, spikes/depressings oblique: >30 degrees perpendicular to long axis spiral: fracture line curves/spirals comminuted: >1 fracture lines that CONNECT segmental: >2 that do NOT connect. each bone complex piece of cortex.

what are the simplest exercises for a recovering orthopedic patients?

slow walking. the slower you walk them, the more likely they will put their foot on the ground, which encourages a normal cycle of loading.

what is an intramedullary pin? when is it used?

smooth edges. placed into medullary cavity of bone, exits cortex at one end. can place in femur, humerus, tibia, and ulna. CANNOT place in radius. partial resistance to major loading forces - generated by bending. doesn't resist compression, rotation. always combine with another fixation method.

what is usually the determining factor as to whether a limb can be salfages?

soft tissue (joints being sparted). if predominantly orthopaedic, can be salvaged.

what are the 4 most common causes of lameness in dairy cows seen by FARMERS? clinical signs, pathology, tx? which one needs systemic AB?

sole ulcers, white line disease, digital dermatitis, foul. in that order 1) SOLE ULCERS: from bruising, horn overgrowth 2) WHITE LINE DISEASE: disease affecting junction b/w sole and wall 3) DIGITAL DERMATITIS: treponemes. footbathing/slurrymgmt. may debride depending on stage. 4) foul (foot rot, but that's different in sheep): f. necrophorum. farms that have a digital dermatitis problem. super-infection of inter-digital face. go deep in the foot, can swell even higher up. the only condition that needs SYSTEMIC ANTIBIOTICS. cows can mask it very well.

what is the pathogenesis of osteomyelitis?

something that disrupts normal homeostasis (pen. injury, infection, etc) - immune response: inflammation change local cytokines. upsets osteoclasts/blasts which disrupts vascular channels, leading to ischaemia. hopefully sequestrum results which is a segment of dead bone (classical example) - osteoporosis adjacent to ischaemia (radiolucent) -osteoproliferation/new bone formation next to it low level: might just thicken periosteum/cortex. aggressive might have pallsading? new bones.

which animals get gout? why? what is the tx?

species that do not have enzyme uricase (humans, birds, reptiles) reptiles get renal damage and then decreased excretion of urate white, peri-articular deposits (urate crystals) lead to an inflammatory rxn. main differential for a lethargic iguana is gout tx: fluid therapy, avoid meds that increase renal excretion

hindlimb bandage horse

splint applied to the lateral side. modified schroder-thomas. hock/proximal tibia fracture.

what is a lag screw?

squeezes 2 bone fragments together. placed at right angles to fracture line. - near cortex is "over" drilled so the screw only grips in the far cortex. as it's tightened, head engages and pulls the near fragment towards the far one. - will not resist loading forces.

how does a CT scanner work? what is a houndsfield unit? what is a narrow window vs wide window?

standard x-ray machine that rotates. the entire system rotates around 360 degrees. patients can move through the machine like a helix to get at 3-D image. hounsfield unit measures CT Opacities via a formula, which can tell you what structure you are looking at. better resolution between soft tissue/fluids. water is 0. NARROW WINDOW = soft tissues only. it is high contrast. don't get bony details. WIDE window: lower contrast - more bone detail.

palpation of horse's back

subjective in regards to where and how hard. symmetry of pelvis (tuber coxae, ischii)

what is the most common tendinopathy in equines? how is it diagnosed?

superficial digital flexor tendinopathy. - palmar metacarpal swelling - initial lameness (variable) - pain on palpation US: "core" lesion. to monitor: can't use lameness to check, because variable. would use X-sectional area measurement and serial ultrasonographic assessment.

what is the zonal structure of articular cartilage?

surface: superficial zone mid zone: aggrecan (proteoglycan) subchondral: becomes more organized as it approaches bone.

how do you surgically perform PROPHYLAXIS for hip dysplasia? (2)

surgery to improve the "fit" of the hip joint. needs to be done early but 50-70% conservative mgmt? PELVIC OSTEOTOMY: (double or triple: cut and rotated so it caputres the ball of the femoral head better). - cut pelvic bone to rotate acetabulum - increase dorsal coverage - stabilise with plate/screws - complications - 4-8 months old JUVENILE PUBIC SYMPHYSODESIS (image) - damage to the growth plate to rotate the acetabulum - < 20 weeks old

what are the main roles of external coaptation? what are its aims?

surgical tx most common. - temp suupport - secondary - primary for some fractures aims: stabilise, elimite forces, allow early wt bearing, and maintain normal joint function

what is proximal suspensory ligament desmitis? clinical signs, diagnostics? (proximal suspensory disease)

suspensory ligament in three parts. proximal most common. history: lameness variable in degree - acute or insidious onset clinical signs: - conformation (hindlimb): STRAIGHT hock, overextending MTP (fetlock) joint - lameness: often lamer with the limb outside of a circle. proximal MC/MT swelling PALPATION: strangulation technique (it's very difficult to palpate in hindlimb). squeeze flexor tendons onto proximal suspensory and look for pain. - diagnostic analgesia - diagnosting imaging: US, radiography, gamma scintigraphy/MRI

observing a horse from a distance during lameness exam: what are you looking for?

symmetry, posture, conformation poor conformation =/ lameness be careful with comments to owners

what is the aetiology of equine laminitis? what are the 3 forms?

syndrome, NOT disease. it's under debate, but associated with systemic disease or excessive wt bearing. three forms: 1) sepsis associated 2) endocrinopathic 3) excessive weight bearing (SLL) from an injury of the opposite leg end result is similar: morphological derangement causes - lamellar separation - DP is no longer suspended in hoof capsule (sinks or rotates) - PAIN

anatomy of a joint? what are the types of synoviocytes?

synovial membrane: - type A = macrophagic type - type B = fibrolast type bone plate underneath cartilage: contributes to progression of OA type II collagen: only found in the articular cartilage

casting pressure

synthetic casting material.

how does DJD progress into OA?

the articular cartilage is eroded and the joint capsule thickens. eventually where the cartilage is eroded, osteophytes form, leading to complete loss of cartilage and bone spurs, and bone lysis.

what are the most common hoof sites of lameness in the horse? what are the only parts that are able to palpate?

the foot. bone and soft tissues inside hoof capsule. inacessible for palaption. only things palpable are dorsal coronary, coffin joint, flexor tendons. difficult to relate: don't try to. neither are nerve blocks.

what is under-running?

the process of d. nososus invading the interdigital skin, breaking the skin-horn junction on the axial wall, and extending underneath the horn tissue medially. this predisposes the foot to infection by f. necrophorum. the soft horn separates from the tissues and the lesion extends anterior and laterally (abaxial wall)

why is a horse's walk not a good gait for detecting subtle lameness?

the time between strides/limb movement is too slow.

why might foot trimming be contraindicated with severe footrot?

the trimmer spreads necrotic material. use farm-dedicated kits.

why do young animals do better with casts? what would you have to consider when casting a very young animals?

the younger the better. very good healing potential, THICK periosteum which keeps it safe. can use them in cases you might not with an older one. can heal a broken leg in 2 weeks. however, becaus they grow so fast, it's possible for them to have malpositioning leading to deformed bones.

what is the anatomy of the cruciates? where do they run and what are the bands?

they are in a cross. cranial: front of tibia to back of femur. caudal: caudal femur to cranial tibia. EXTRAsynovial - sealed in by synovium. BANDS: looks like there are two bands. they are both taut in extension, and craniomedial taut in flexion. can test for partial vs. complete cruciate tear.

what is the canter? what is it used for?

three-beat gait, with lead preference - difficult to identify subtle lameness - useful for back/rider/saddle assoc/ problems or performance problems

forelimb division 1: coronary band to distal metacarpus. how to immobilise?

to avoid flexing component of suspensory: align dorsal cortices. STAND HORSE ON TIPTOES to avoid pull of flexor/suspensory. KIMZEY splint, padded bandage/cast bandage. make sure not too heavy (pendulum). under DEBATE. some argue that it's counterproductive.might displace a fracture that is otherwise stable. want you do use it at normal fetlock angle. fracture gap opens. more difficult in the hindlimb. both are being done in the field. some form of coaptation.

how does the MRI grayscale work? how does it vary between T1 and T2 weighted images?

totally different process, therefore different scale. hypointense: air, cortical bone. medium: soft tissues high: fat. in T1, water is HYPO intense (dark) in T2, it's HYPER intense. (white) you can differentiate by looking for areas with high water content and seeing if they are hypo/hyperintense.

what is the travel vs. action of a horses' limb? what are the phases of stride?

travel: flight of single hoof in relation to other limbs, often viewed from side or from behind action: overall description of gait characteristics - takes into account joint flexion, stride length, suspension and other qualities - variation between different types and breeds phases of stride: landing, loading (fetlock drops), stance (fetlock comes back up), breakover (heel lift) then toe pivot, swing

what is the medical therapy of equine laminitis? how does it vary depending on aetiology?

treat ASAP - emergency. analgesia: - NSAIDS the mainstay: cheap, can be given orally. PBZ (cheapest, longterm), flunixin, etc. iv or oral. - opiates: morphine (1-3 hrs) pethidine, fentanyl. controlled, short acting, side effects. more likely for a hospital situation (have to inject, short half-life) vasodilation: endocrine, wt-bearing ACP, historically. they thought it was about ischaemia, not inflammation. it can help because it makes them tired and then they lie down, rest. doesn't actually help via vasodilation. vasoconstriction (sepsis-associated): Ice, chill, 10 degrees C. no complications. foot support: essential. - increase bedding - frog support: bandages, lilypads, NFS - frog AND sole support: foam, dental impression material, etc. mgmt: box rest diet: no grass, 1.5-2% poor quality hay. no/minimal concentrates, HiFi, unmollassed sugar beet. endocrine therapy: - PPID: pergolide (dopamine receptor agonist) - EMS: weight loss, exercise, +/- pharmacological agents

what is septic pedal osteitis? how is it treated?

treat by debridement/curretage, wound care.

immobilisation of elbow to scapula (forelimb)

triceps apparatus disabled. elbow cannot be fixed for wt. bearing - "dropped elbow". difficult to walk. can't bring the limb foreward. goal: splint carpus in extended position to allow for wt. bearing/ balance. "peg-leg". - padded bandage with splint caudally or cranially over carpus. - walking may be difficult, foals may be too weak ton ambulate.

step 2 of foot trimming

trim 2nd claw to match correct length of 1st claw. weight-bearing claw grows more than non-weight bearing. that leads to excess horn growth, pressure points, lameness. stimulation of weight bearing which causes growth.

how does trimming affect the horse's balance?

trimming INCREASES surface area of contact, uniformity of wall contact. - increase contact peripheral sole - more even load distribution. example: egg bar shoe (image)

what is the gait preferred for lameness exam in horse?

trot: two beat, diagonal gate. steadiest, most rhythmic. good for subtle lamenesses.

what are the common primary neoplasms of the digit? how do they present? how should you diagnose and treat?

type: 12% of all subungual masses are tumours, and 60% of those are malignant. - SCC most common, then melanoma >STS > MCT > OSA. present with lameness, mass lesion, or ulceration. diagnosis: radiographs, staging, sampling tx: amputation. Px depends on tumour type and tissue of origin but they can often do just fine.

how might you examine the back of an eye in a dog with cataracts? why would you do this?

ultrasound exam of the retina, etc. to see if the eye is fit for cataract surgery.

what are the pathologies involved in elbow dysplasia?

umbrella term - several pathologies. now "developmental elbow disease" MEDIAL COPARTMENT DISEASE = 1) fragmented medial coronoid process/medial coronoid disease 2) osteochondrosis humeral trochle 3) ununited anconeal process (UAP) can also get joint incongruity. all cause OA.

what is the carpal flexural deformity? how is it treated?

unable to extend/lock carpal. tx: responds well to conservative treatment. - exercise, physiotherapy - tube casts if severe to keep leg str8, weaken tendons, allow extension - surgery??

OCD of the humerus: signalment, history, diagnostis?

uncommon. lab/goldens, newfoundlands. more common in males, rapid glrowth, high E diet, Ca:P ratio - 90% bilateral pathology: osteochondrosis and flap development (like shoulder) CrCd Radiograph best - medial trochlea + humeral condyle - CT : bone reacted to it as well (sclerosis) Tx: none? flap removal, forage, micropick for bleeding. bad prognosis

how do you reduce the weight of a shoe? when might this benefit a horse?

use aluminum alloy. - absorbs high frequency vibrations better - better grip on hard compact ground - causes less fatigue - reduces hyperflexion of limb in air b/w stance phase - may benefit patients with articular and tendon/suspensory ligament lesions

how should you deal with hoof cracks? what are aetiology? where are they normally found?

usually longitudinal axis. due to: poor horn quality, thin hoof wall, or abnormal angles/balance repair methods: debride, fill with acrylic/shoe. various fixing devices (plate, tension wires). overgrown feet can propogate into foot imbalances.

HINDLIMB 2 (THE HIP): which animals are more likely to get hip dysplasia?

very common in large breed dogs/medium breeds, despite breeding schemes. rare in cats. - labs, GSD, goldens. rarely giant, small breeds, or cats. - most commonly labs. strongly genetic - HIGH HERITABILITY - polygenetic + environmental influence (diet, exercise may affect signs). elbow is 50-70, hip is 20-30 Heritability however ad lib fed dogs had an earlier onset with increased severity.

what is sepsis-associated laminitis? what is the aetiology?

very sick horse!!! GI/Pneumonia/Septic. similar to SIRS stuff gets into the foot (endotoxin) sets off inflammatory cascade, and ends in organ dysfunction. just HAPPENS to be in the foot. it will be elsewhere as well. - systemic inflammation , endothelial activation, leucocytes, cytokines, oxidative injury, etc. - MMP (matrix metalloproteinase) activation not the initiating event. older research says that. instead it's failure of hemidesmosomes (LBE cell function caused by hypoxic/inflammatory injury) two experimental models: carb overload, black walnut

examination of the injured horse lmb

visual: deviation, hyperextension (breakdown injuries of fetlock support apparatus or transection of DDFT), swelling/haematoma, open wound. palpation: crepitus, fracture fragments, open wound/moist spot on palpation. rough localistion/classification of fracture, technically feasible.

when to quarantine for footrot?

when there is NO footrot present in the flock. put in place until climactic conditions have been suitable for transmission for 2-3 weeks (long enough for them to show signs of disease) after: inspect sheep, no point foot-bathing, vaccinating, etc

how does density and exposure related on an xray? how does film vs. digital vary?

xray exposure determines film density. low exposure is very white. too much exposure is too dark. there is a narrow image. FILM: underexposed gives noise. DIGITAL: wider exposure range, more linear and less logarithmic. you can alter the density/opacity after processing.

how can you determine what the distance of something is with an ultrasound? (how does the machine produce an image?)

you know the velocity of the wave and the time it took. D = V + t/2. the machine does these calculations for you and produces an image.

what breeds are predisposed to elbow dysplasia?

young medium-giant breeds (smaller chondrodystrophic dogs) - 35% bilateral heritability: rottweilers, retrievers, bernese mountain dogs. there are screning programs. MOST COMMON = MEDIAL CORONOID PROCESS DISEASE (95%).

radiographs of MCP disease? treatment? prognosis?

young: may look normal. older: OA change, and then diagnosis of exclusion. may see changes/remodelling at MCP. CT: sclerosis, fissures, non-displaced, OA. lots of different phenotypes. Tx: conservative (see OA mgmt) - wt restriction, regular exercise (frequent short walks), hydro, NSAIDS, omega-3 - no clear long term diff. b/w this and surgery - arthrotomy/arthroscopy. remove fragment, reduce size medial coronoid (grind it away to reduce loading) - more rapid improvemtn - ulna osteotomy to change loading in elbow (uncommon) prognosis: - arthroscopy: 50% resolve, 20% improve.

what are main ddx for shoulder lameness in dogs? young vs. old

young: osteochondrosis dissecans (OCD) - condition of developing cartilage and supporting bone. - fast growing, high performance patients. Large/giant breeds (great danes, wolfhounds, bernese mountain dogs), males > females, 50% bilateral - multifactorial - dogs: elbow, shoulder stifle tarsus. older: shoulder OA, shoulder soft-tissue injuries - "rotator cuff"