Final Flashcards
Collagen in hyaline cart
Type II collagen
What makes hyaline cart
ECM and chondrocytes
What makes ECM
70% water, type II collagen, proteoglycans
What is aggrecan
Major ECM proteoglycan made of chondroitin and karatan sulfate
Fxn type II coll
Counteract tensile forces
What is a proteoglycan
100 GAGs on a protein core, arranged on a hyaluronan mol
GAG fxn
Negative charge attracts water to counteract compressive forces
Functional layer of synovial memb
Intimal- cells that perform fxn
Type A synoviocyte
In intimal layer, phagocytic
Type B synoviocyte
In intimal layer, secretes proteins, filters plasma to make fluids, releases cytokines
Predom cell in normal synovial fluid
Mononuclear
Viscosity of syn fluid from
Hyaluronan molecules (large)
MMPs
degrade ECM, released by chondrocytes and synovio’s in inactive form
Name MMPs
collagenase (mmp-13), gelatinase, stromelysin
Stromelysin
MMP that degrades proteoglycan part of ECM
MMP inhibitor
TIMP and tetracycline
IL-1 and TNFa fxn
Inflam cytokines- inc catab (up-reg MMPs, PGs, free radicals and each other)
IL-1 fxn
Inhibit TIMP and IL-1Ra (its own inhibitor)
IL-1Ra
IL-1 Receptor antagonist
First biomechanical damage in injury
loss of proteoglycan leading to collagen degradation, hard to regen
Intrinsic cartilage healing
Poor- from chondrocyte synthetic activity
Extrinsic healing-
From bone marrow sources, makes fibrocartilage NOT type II
Matrix flow
Healing by spread/thin/melt of cartilage
OC is what type of dz
Developmental orthopedic disorder (DOD)
Most common CS of OA
pain, lameness
OA- type of dz
trauma/degen
Tissue changes in OA
cartilage damage, synovitis, capsulitis (decreased ROM), ligament/menisc injury (dec stability)
Abnormal force on normal cartilage=
intra-artic fx
Normal force on abnormal cartilage=
wear and tear (normal)
Anatomy confers___ and physiology confers____
mechanics, biology (catab/anab balance, dz response)
OA rads-
No joint space=no cartilage!, subchondral bone sclerosis/lysis
Enthesiophyte
Formation of bone at capsule and ligamentous attachments
Osteophytes
bone form at articular margin
Gold standard dx OA
Arthroscopy bc rads may not show changes early
Fluid analysis in OA-
Cytology not useful, THIN IS BAD
Microfracture
Tx for OA makes holes in subchondral bone to stim extrinsic heal- NOT type II, fibrocart
Arthrodesis Px
High motion- poor, salvage; low motion- may return to fxn (distal tarsal, pastern)
Most common NSAID
Bute- flunixin not as good
Good long term NSAID
Fircoxib- more cox 2 selective so less SE, but less effective
Corticosteroid tx for OA
Intra-articular (methylpred for high motion, triamcinolone for low)
Hyaluronan - route
IA/IV
What is adequan
polysulfated GAGs
IRAP
Bio therapy for OA to block IL1 receptors
What is always an emergency
Septic arthritis
Types of septic arthritis
Traumatic (from wound entry), hematogenous, iatrogenic
Three types of hematogenous septic arthritis in foals
SEP: S- synovial memb source, E- subchondral bone of epiphysis into joint, P- physeal
Synovial fluid analysis in septic arth
WBC >30k, >90% degenerative neuts, +/- TP >2
Iatrogenic septic arth org
Staph Aureus
Trauma septic arth org
enteric gram negatives
CS- septic arth, young and adult
young- systemic, painful; mature- swollen joint, usually not painful
Tx septic arth
Synovial lavage with balanced electrolyte solution +/_ DMSO; broad Abx (IA intermittent best concentration at synovium)
Describe stopping septic arth tx
WBC not accurate, will stay higher, use imporvement in effusion and lameness, stop pain control before Abx to assess fully
Hyperextension of canine limb, adduction of elbow, circumduction of distal limb with carpal flip
Infraspinatus contracture from fibrosis in working dogs
Infraspinatus contrcture tx
infraspinatus tenotomy- cut infraspin tendon
Scapulohumeral luxations- types, which more common
Medial (smaller dogs, congenital), lateral (larger dogs, less common)
Scap-hum lux- medial - sx types, which better
Open or closed reduction, open better, closed re-lux
What makes tx for Scap-hum luxation successful
Normal anatomy of glenoid still viable- if not, must arthrodese joint
Open scap-hum- medial: reduction- method
Use biceps brachii tendon as support to replace ruined collateral ligaments
Bandage for scap-hum sx
Spica
Scap-hum lux- Lateral: Sx
Closed with spica possible, open same as medial (biceps brachii tendon replacing lateral collaterals)
Bicipital tenosynovitis- signalment, presentation
Large breed, working dogs, chronic intermittent forelimb lameness (overdx) (biceps tendon goes through joint, long term wear and tear= lose integrity)
Tx bicipital tenosynovitis
1-2 steroid inj into tendon within joint, if returns, transect tendon at attachment- Popeye procedure
Dx bicipital tenosynovitis
U/S helpful for fluid pockets, etc; Pain on direct pressure to tendon while flex shoulder, extend elbow
What way do traumatic elbow luxations occur
R and U go laterally to humeral condyle bc trochlea more distal than capitulum
Dx traumatic elbow luxations
Rads- orthogonal view, bc easy to miss on lateral!!!
Tx traumatic elbow luxations
REDUCE ASAP, closed preferred
traumatic elbow luxation sx- describe 4 steps
Flex to reduce anconeal, roll radius in, maintain in extension to lock anconeal in- spica to keep in extension (2 weeks)
Congenital elbow lux- signalment
Small breed and bulldogs
Tx Congenital elbow lux
early sx
Angular limb deformity- etiology, location
Premature closure of GP in antebrachium; distal ulnar physis, gives radius curvus due to tethering of paired bones
What must you do in elbow trauma of
Document want owner back in 3 weeks for rads to ensure no GP damage
Canine carpal hyperextension injury- etiology
Large, working- trauma > degen, tear carpal ligaments (palmar fibrocartilage plate)
tx Canine carpal hyperextension
COAPTATION WONT WORK- pancarpal arthrodesis needed in 90%
Most common sites of OCD
Caudal humeral head! humeral condyle, lateral femoral condyle, talus
OC- describe
Developmental, disturbance of normal endochondral ossification in young causes THICKENED CARTILAGE where bone not forming, bc so thick, unhealthy bc poor blood supply
OCD-
Sequelae to OC, crack present, communicates with joint
Signs of OC/OCD on rads
OC- flattened/concave subchon bone; OCD- no different, flap cant be seen! soft tissue opacity
OC- tx
NOTHING
OCD progression- where is lameness most often
Shoulder or elbow
Dx OCD in shoulder
Pain on flexion and extension
Tx OCD
Remove the flap- arthroscopy preferred
Elbow dysplasia conditions
UAP, OC/OCD of hum condyle, FCP
Elbow dysplasia from FCP- signalment
Rottweiler
UAP- describe
Failure of fusion of anconeal process to olecranon
UAP- dx
Extended and FLEXED view of elbow to see anc proc within hum condyle
UAP- signalment
males, GSD or basetts
UAP- causes
R/U incongruity- ulna too short
Tx UAP
caudal arthrotomy (excise A.P), fuse (young, not dz’d), prox. diaphyseal ulnar osteotomy- to allow it to lengthen ulna, relieve pressure, cause fusion
OCD of humeral condyl- location, signalment
Medial, chocolate labs
Dx humeral condyle OCD
Cranio-lateral, Caudo-medial oblique rads (with lateral, CC, flexed)
Most common elbow dysplasia disease
FCP
FCP etiology
RARELY traumatic- usually repetitive cyclic loading- ulna narrow concavity, step from short radius
FCP- dx
Biggest clue: DJD of medial elbow compartment (rads not great but lateral view- secondary DJD changes in absence of UAP or OCD
Inherited elbow dysplasia conditions-
FCP and OCD
Panosteitis- signalment, findings
young, large, growing dogs; palpation painful at metaph/diaph region
Panosteitis- CS
Shifting lameness, SYSTEMIC SIGNS
Panosteitis- describe, dx
hypervascular response in medullary a/v, Rads: increased opacity on rads; IDIOPATHIC, SELF RESOLVING
Define hip dysplasia
Abnormal development (often too fast) of CF joint causing laxity and leading to OA (
Hip dysplasia key initial feature
Joint laxity before CS from OA
Hip dysplasia - dx
Ortolani test
OFA vs PennHip
OFA subj/min 2yr, Penn- obj, any age
TPO- parts
Ilium, ischium, pubis
Juvenile symphysiodesis
Improve acetabular coverage dorsally via premature closure of GP
Hip dysp goals
Young- prevent DJD, elim pain; Old- elimin OA pain
Three major stabilizers of hip
Round ligament, joint capsule, dorsal acetabular rim geometry
Traumatic hip lux- classification
Craniodorsal (SOME ventral)
Dx hip lux
CrDorsal- needs two views to diff’ate lux from sublux, underlying dysplasia
Best Tx hip lux
Toggle pin
Primary restraints- stifle
Cr and Ca cruciates, Mand L collaterals
Cr Cruciate job
Prevent displacement of tibia cranial to femur
Chronic CCL degen rupture- cause
Chronic repetitive fatigue of ligament
Concurrent injury with CCL
Medial meniscus- CAUDAL HORN crushed by femoral condyle sublux
Dx CCL rupture on rads
JOINT EFFUSION (no longer fat opacity)
Patellar lux grades
IN/IN, IN/OUT, Out/In, out/out
Tibial osteotomy- result
For CCL rupture, neutralize tibial thrust
TPLO-
MOST COMMON CCLr, reduced angulation of plateau
Most common patellar lux-
Medial, small dogs
Sx for patellar lux IF
CS at home
Trochlear wedge recession
Remove osteochondral block, then replace after removing bone underneath- for patellar lux
Patellar sx options (2)
Tighten laterally or release medially
OCD hindlimb- locations
Lat fem cond, medial troch ridge of tallus (STILL MORE COMMON IN FORELIMB)
Tx- OCD hindlimb
Flap excision > conservative mgmt
Hip dysplasia sx indications
Young:: TPO, JPS; Old: FHO (salvage), total hip