Synovitis & Degenerative Joint Disease, up to fetlock Flashcards

Question

Neutraceuticals -Chondroitin sulphate for Synovitis & Degenerative Joint - what is it? - use? - efficacy?

Answer 1

* Component of cartilage matrix * Used alone not beneficial * Combination of chondroitin & glucosamine given to 15 veteran horses for 3 months – after 8 weeks, range of motion and stride length was significantly increased

Answer 2

* ASUs (=avocado and soybean unsaponifiable extracts) * Lameness scores, joint effusion, inflammatory parameters were unchanged * Post mortem showed less cartilage erosion, and less synovial hemorrhage * Total GAG content in cartilage higher

Answer 3

* Part of extracellular matrix (elasticity) * Synthesized by chondrocytes & synoviocytes * Function: – Viscoelasticity of joint fluid & lubrication – Reducing cell migration – Decreasing rate of diffusion & flow of solutes – Anti-inflammatory due to “steric hindrance” (slowing of chemical reactions) - reduce chemotaxis by increasing phagocytosis of activated neutrophils - Clinical efficacy of IA HA demonstrated in multiple clinical reports

Answer 4

HA in the range of 0.5 to 2.0 x 106 d is ideal

Answer 5

- yes seems to be at least as an anti-inflammatory * Reduced lameness, less synovial inflammation, lower TP, reduced PGE2 = effect on synoviocytes * No effect on cartilage itself

Answer 6

* Mechanism of action – unknown * Inhibits degradative enzymes involved in OA * Anti-inflammatory role by reducing leukocyte migration & interleukin levels * Biosynthetic role – increases HA, GAG, collagen content

Answer 7

* Evidence of IM efficacy not strong * Efficacy demonstrated particularly for IA * Drawback for IA administration is increased risk of sepsis * Inhibits complement activity in the joint * Incidence much lower when combined with amikacin

Answer 8

* Decreases osteoclastic bone resorption <><> * Clinical outcome subjectively improved for: * navicular disease * small (distal) hock joint OA * DJD of the spine

Answer 9

– Reduce capillary dilatation, margination, migration & accumulation of inflammatory cells – Inhibit synthesis & release of inflammatory mediators involved in development of OA (eg prostanoids, nitric oxide) – Pain relief = reduction of prostaglandin due to inhibition phospholipase A2 and cyclooxygenase (COX) 2 inhibition – Also disease modifying!!!! * Suppress TNFα and IL1 at low concentrations – these are the most cartilage destructive enzymes * Inhibit other mediators involved in OA at low doses

Answer 10

– Worry that pain free joint may accelerate cartilage degeneration – High dose inhibits proteoglykan synthesis & negatively affect collagen organization BUT only low levels needed for scavenging mediators – REST is needed after injection (increased rest in people increased treatment efficacy by 70 %)

Answer 11

– Methylprednisolone acetate (Depomedrol) – Triamcinolone acetonide – Betamethasone acetate <><><> - for steroids, less is more > want to avoid cartilage damage

Answer 12

= Interleukin-1 Receptor Antagonist Protein * In OA, interleukin 1(IL1) , a proinflammatory cytokine, induces matrix degeneration * Healthy joint = balance between IL1 & IL1 antibody - expensive but usually effective, if client wants to spend money do this instead of steroids

Answer 13

High load – low motion joints * Small hock joints (tarsometatarsal & distal intertarsal joints) * Interphalangeal (Coffin/Pastern) Joints <><> High motion – lower load joints * Fetlock * Carpus * Stifle (femorotibial joint)

Answer 14

Ø Theory that nutrient and waste exchange less efficient in these joints because forces distributed over a smaller area (↑ pressure). Ø May result in cartilage trauma (overload?) & perpetuated by trauma > INFLAMMATION

Answer 15

Ø Cartilage necrosis Ø Focal destruction of subchondral bone/ sclerosis Ø Periosteal new bone & enthesiophyte production Ø Ankylosis (complete/ partial) in advanced stages Ø Advanced cases → bony enlargement

Answer 16

Ø “High Ring Bone” = DJD pastern joint Ø “Low Ring Bone” = DJD coffin joint

Answer 17

- Lameness → mild to severe. → acute or insidious onset. <><> - Diagnostic Analgesia Ø Abaxialsesamoid block. Ø Synovial anesthesia of coffin or pastern joint

Answer 18

Ø Rest, NSAID’s and other medications as needed, initially. Ø Intra-articular medications often quite helpful. Ø Proper foot trimming and good shoeing. Ø Surgical arthrodesis of PIP joint. Ø Alcohol facilitated arthrodesis ???

Answer 19

Ø a.k.a. Distal tarsitis or “bone spavin”. Ø Tarsometatarsal (TMT) and distal intertarsal (DIT) joints. Ø The most frequent and important cause of hind limb lameness in general. Ø Typically, horses have an insidious onset of hind limb lameness, over a variable period. Ø A “classic” history is that the horse “warms-out” of the lameness as exercise progresses. Ø Horses tend to exhibit a shortened cranial phase of the stride and may stab or scuff the toe. Ø Upper limb flexion positive

Answer 20

- remodelling (subchondral sclerosis and osteolkysis) and osteophyte formation - as the disease advances, decreases in joint space will become evident - slab fractures of T-3 and T-C can be present.

Answer 21

§ Early: Rest, NSAID’s, systemic & IA medications. § The distal tarsal joints may be the most frequently injected joints in athletic horses.

Answer 22

§ Frequent IA corticosteroid therapy in certain horses? § IA 70% ethyl alcohol → initial clinical/experimental data encouraging.

Answer 23

§ Transarticular drilling → 70-80% success rate. § Transarticular laser ablation. § Arthrodesis using small bone plates.

Answer 24

§ Easily managed with IA medications in the early stages. § If you want to chemical arthrodese, more success if done early § Post operative success varies with each case and the horse’s use.

Synovitis & Degenerative Joint Disease, up to fetlock Flashcards

(48 cards)