EXAM III: Pathophysiology and Treatment of Osteoarthritis and Developmental Orthopedic Disease Flashcards
Barton
joint disease
To describe the basic physiology of cartilage and structures within joints
What is cartilage made up of?
What happens when inflammatory changes take place?
What inflammatory changes occur?
Basically, the cartilage is made up of proteoglycans (which are proteins with heparin sulfate chains and glycosaminoglycans) and water, the dry weight is made up of proteoglycans and type II collagen.
When mechanical forces act on the cartilage, there is stress, inflammation, decreased sf viscosity, and cartilage breakdown.
how does this happen? let’s take it down to the cellular level where the synoviocytes live, they get the sense of trauma and inflammation and start to release IL-1, TNF-alpha, prostaglandns and metalloproteinases. This is released into the synovial fluid which is then released in the articular cartilage where chondrocytes then release PGE2 and mettaloproteinases which THEN release stromelysin collagenase causing MATRIX DEGRADATION.
* it’s a self sustaining process.
joint disease
What tools do we have to diagnose OA? When are some more useful than others?
exploratory arthroscopy can also be therapeutic, but there are also of course radiographs, nuclear scintigraphy which is good for stress factors, ultra sound, and MRI but in an MRI, you can only scan distal to the tarsus or carpus, MRI is not available for the stifle.
joint disease
What are some systemic, intra-articular, and chondroprotective therapies you can offer a hrose with OA?
NSAIDs? Steroids? Types? What are side effects?
Of course, we have our NSAIDS: (vetri)bute [phenylbutazone], banamine, and equiox (equiox has less inhibition of cox 1. phenylbutazone is still the most popular becasue its cheaper than equiox.
There is also polysulfated glycosaminoglycan (adequan) which stimulates the production of hyalauran (synoviocytes), increases synthesis of proteoglycans and collagen by chondrocytes, and inhibit metalloproteases, cathespins, and other degradatibe enzymes.
Intra-artiular therapies include: corticosteroids (steroids work one step before NSAIDs), HA, and biological therapies. rmeember, steroids work great but come with GAG depletion, suppression of collagen and HA synthesis, laminitis, and steroid arthropathy.
Triamcinoloe Acetonide (Vetalog) is the best steroid choice. Methylprednisolone acetate (depo(medrol)) comes with severe detrimental effects that affect healthy cartilage. Betamethasone has similar effects.
joint disease
What alternatives do horses have to steroids?
systemic therapies? topical therapies?
Sodium hyaluronan, has the best effest when used to treat acute synovitis, combines effects with low dose steroids, MOA unclear but lubrication, steric exclusion of particles and anti-inflammatory effects are noted.
Pick something over 500,000 daltons (Hyvisc, Hylartin V, Legend IV (requires more dosing))
There is also a liposomal NSAID cream. * Surpass. The liposomes enhance local absorption of the active ingrediant, diclofenac, at the site of inflammation. “significant” improvement in lameness. it is also disease modifying in that it improves gross cartilage staining and improves total articula glycosaminoglycan content and bone sclerosis.
don’t forget rehab!!
developmental disease
What physiology leads to osteochondrosis
how can osteochondrosis present?
Ostechondrosis can present in two ways: as osteochondritis dissecans (OCD, when there is a cleft formation in thickened cartilage after endochondral ossification) and subchondral bone cyts/cystic lesions (SBC/SCL, when there is entrapped cartilage after endochondral ossification)
developmental disease
Be able to name the diseases classified under Developmental
Orthopedic Disease (DOD)
What diseases are classified under DOD?
What causes the changes in OCD, physitits, angular limb deformities and flexural limb deformities?
- Physis matures too rapidly = Contracted Tendons
- Physis becomes inflamed = Physitis
- Physis has abnormal mechanical pressure = ALD
- Epiphysis has abnormal ossification = OCD
your patient is a young horse with the following clinical signs:
* Young horse, often fast growing
* Joint effusion
* Variable lameness present
* Often bilateral involvement
* Lateral trochlear ridge, medial
trochlear ridge
What is your top differential?
OCD (in the stifle)
A horse has a subchondral bone cyst, it is almost always on the ___________
medial femoral condyle.
Flexural limb deformitiesoften involve the DIP or fetlock joints, which is more common at birth (to 4 months)? in yearlings?
What can predispose horses to this disease?
What treatments can be offered?
DIP at birth to 4 mos
MCP in yearlings
congenital: teratogenic, intrauterine positioning, genetic predisposition (rapid growth)
Acquired: nutrition trauma, infectious polyarthritis (all of these would be painful and have altered weight bearing)
Treatments:
* Evaluate nutrition, control growth rate
* Control painful stimuli
* Medical treatment
( Oxytetracycline, Splinting)
* Surgical intervention
You are presented with a
newborn foal with carpal
contracture meaning it
cannot stand without
assistence
What are your initial
treatments in regards to the
orthopedic disease?
What was the most likely cause?
oxytet and splint from elbow to ground
likely cause, uterine malpositioning
Define valgus and varus limb deformities.
What predisposes a horse to these deformities?
in corrective trimming, which sides do you trim?
Valgus deformity =
LATERAL deviation of
the limb distal to the
site of the deformity.
trim medial side of foot.
Varus deformity =
MEDIAL deviation of
the limb distal to the
site of the deformity.
trim lateral side of foot.
incomplete ossification of the cuboidal bones or epiphyses or ligament laxity (medial, lateral collateral ligaments of joints)
You’re considering surgical intervention on a young horse with angular limb deformities. The horse owner wants to wait a few weeks to see if the problem self corrects, what do you say to the owner?
when it comes to surgical treatment, you must act before the physis closes.
distal to the radius/ tibia the best therapeutic window is within 4-6 months. The final closure is at 1-1.5 years.
in the distal metacarpus/metatarsus the best therapeutic window is within 3-4 weeks. The final closure is at 12-14 weeks.
a horse presents for carpus varus. the limb is palpated for laxity. the limb can be corrected manually. Could you say then that this deformity originates from the growth plate?
No, the bones could be pushed in due to laxity.
You want to surgically insert a transphyseal bridge to correct an angular limb deformity, which side should the bridge go on>?
bridge the side you want to slow down the growth.
for valgus, because they are turning laterally, the medial side is the faster growing side so, therefore you would bridge the medial physis.
bridges are removed
