DJD Flashcards
what two things cause morphological breakdown of the articular cartilage
abnormal stress on normal cartilage,
normal stress on abnormal cartilage
what are the bad guys in DJD inflammation
IL-1 and TNF alpha degrade cartilage/matrix
this causes more of them to release from the cells, viscous cycle
why are the cytokines produced in the joint
trauma and inflammation to the synoviocytes cause cytokine release and these attach the articular cartilage chondrocytes
who are the good guys during DJD
TIMP - active collagenase and growth factors- acting on the chondrocytes
serine proteinase inhibitors
what are the bodies natural responses to OA
limit ROM to limit the pain
articular cartilage breaks down and stops producing collagen
why do we care about articular cartilage degration
reduced compressive and tensile strength
how does IRAP work
competes with IL-1
how does the bone respond to all of this
bone sclerosis and thickening where there is increased load/stress– this decreases the ability to absorb shock
three big takeaways about DJD
multifactoral
permanent
intervene early
what are the goals of treatment for DJD
decrease inflammation, lubricate joint, halt disease, alleviate pain
what are the two essential clinical features of OA requiring attention
pain and loss of function
conservative approach to managing OA
exercise modification, weight reduction, antiinflammatories, SC
what is the best mode of treatment for OA
joint injections
what is adequan
PSGAG, stimulates production of HA, increase PG and collagen
what is the coctail for intraarticular medications
steroids, HA, regenerative medicine
big disadvantage with intraarticular steroids
laminitis, risk of infection and steroids dull the reaction
steroid of choice? and one we never use?
triamcinolone
depo-medrol (methylpred)
we suspect a post injection flare- heat, pain, swelling. what is our other ddx, and what do we do
infection, refer to surgeon to tap
if not willing to refer, try treatment and abx
how long do we worry about a post joint injection infection
as long as 2 weeks, steroids will dull the response and WBC are not as high as you would expect
HA is most effective in treating what
acute synovitits
what is polyglycan approved for
replacement of joint fluid following scope
what to remember about giving PSGAGs
do not give with steroids
what is the disadvantage of PRP
they have increased leukocytes which can cause more inflammation
how does IRAP work
competes with IL-1 for receptors– receptor antagonist
BM or Ad cells
no improvements seen
what joint is diagnostic arthroscopy almost always warranted
stifle
what is the primary goal of arthroscopic techniques for OA repair
enhancement of the repair
remove loose cartilage and bone,
remove calcified cartilage
microfracture
what is the requirement for extrinsic repair
removal of the calcified cartilage so new cartilage can form in the defect space
what techniques do we use for extrinsic repair
microfracture through subchondral bone to increase blood flow to the area and get better quality healing
what joints can be fused adn still maintain function as an athlete
distal tarsal -DIT, TMT, Pastern PIP,
Coffin- not commonly done
what joints can we fuse as a salvage procedure to be pasture, breeding horse
fetlock- MCP/MTP
carpal- partial or pan
how does laser arthrodesis work
heat kills the chondrocytes and damages the nerves
for a pastern (PIP) arthrodiesis, which has a better prognosis
hind better than front.
why is fetlock arthrodiesis tough
the plate is on the dorsal aspect and the biomechanics work against the plate
what are the classic radiographic signs of DJD
decreased joint space, osteophytes, lysis and sclerosis, enthesopathy
horse is lame, you radiograph the hock and find fusion in the joint space, what do you do
since it is fused would this cause lamenes/pain? unlikely. do your blocks and look for another cause
