Final Flashcards
(123 cards)
1
Q
Collagen in hyaline cart
A
Type II collagen
2
Q
What makes hyaline cart
A
ECM and chondrocytes
3
Q
What makes ECM
A
70% water, type II collagen, proteoglycans
4
Q
What is aggrecan
A
Major ECM proteoglycan made of chondroitin and karatan sulfate
5
Q
Fxn type II coll
A
Counteract tensile forces
6
Q
What is a proteoglycan
A
100 GAGs on a protein core, arranged on a hyaluronan mol
7
Q
GAG fxn
A
Negative charge attracts water to counteract compressive forces
8
Q
Functional layer of synovial memb
A
Intimal- cells that perform fxn
9
Q
Type A synoviocyte
A
In intimal layer, phagocytic
10
Q
Type B synoviocyte
A
In intimal layer, secretes proteins, filters plasma to make fluids, releases cytokines
11
Q
Predom cell in normal synovial fluid
A
Mononuclear
12
Q
Viscosity of syn fluid from
A
Hyaluronan molecules (large)
13
Q
MMPs
A
degrade ECM, released by chondrocytes and synovio’s in inactive form
14
Q
Name MMPs
A
collagenase (mmp-13), gelatinase, stromelysin
15
Q
Stromelysin
A
MMP that degrades proteoglycan part of ECM
16
Q
MMP inhibitor
A
TIMP and tetracycline
17
Q
IL-1 and TNFa fxn
A
Inflam cytokines- inc catab (up-reg MMPs, PGs, free radicals and each other)
18
Q
IL-1 fxn
A
Inhibit TIMP and IL-1Ra (its own inhibitor)
19
Q
IL-1Ra
A
IL-1 Receptor antagonist
20
Q
First biomechanical damage in injury
A
loss of proteoglycan leading to collagen degradation, hard to regen
21
Q
Intrinsic cartilage healing
A
Poor- from chondrocyte synthetic activity
22
Q
Extrinsic healing-
A
From bone marrow sources, makes fibrocartilage NOT type II
23
Q
Matrix flow
A
Healing by spread/thin/melt of cartilage
24
Q
OC is what type of dz
A
Developmental orthopedic disorder (DOD)
25
Most common CS of OA
pain, lameness
26
OA- type of dz
trauma/degen
27
Tissue changes in OA
cartilage damage, synovitis, capsulitis (decreased ROM), ligament/menisc injury (dec stability)
28
Abnormal force on normal cartilage=
intra-artic fx
29
Normal force on abnormal cartilage=
wear and tear (normal)
30
Anatomy confers___ and physiology confers____
mechanics, biology (catab/anab balance, dz response)
31
OA rads-
No joint space=no cartilage!, subchondral bone sclerosis/lysis
32
Enthesiophyte
Formation of bone at capsule and ligamentous attachments
33
Osteophytes
bone form at articular margin
34
Gold standard dx OA
Arthroscopy bc rads may not show changes early
35
Fluid analysis in OA-
Cytology not useful, THIN IS BAD
36
Microfracture
Tx for OA makes holes in subchondral bone to stim extrinsic heal- NOT type II, fibrocart
37
Arthrodesis Px
High motion- poor, salvage; low motion- may return to fxn (distal tarsal, pastern)
38
Most common NSAID
Bute- flunixin not as good
39
Good long term NSAID
Fircoxib- more cox 2 selective so less SE, but less effective
40
Corticosteroid tx for OA
Intra-articular (methylpred for high motion, triamcinolone for low)
41
Hyaluronan - route
IA/IV
42
What is adequan
polysulfated GAGs
43
IRAP
Bio therapy for OA to block IL1 receptors
44
What is always an emergency
Septic arthritis
45
Types of septic arthritis
Traumatic (from wound entry), hematogenous, iatrogenic
46
Three types of hematogenous septic arthritis in foals
SEP: S- synovial memb source, E- subchondral bone of epiphysis into joint, P- physeal
47
Synovial fluid analysis in septic arth
WBC >30k, >90% degenerative neuts, +/- TP >2
48
Iatrogenic septic arth org
Staph Aureus
49
Trauma septic arth org
enteric gram negatives
50
CS- septic arth, young and adult
young- systemic, painful; mature- swollen joint, usually not painful
51
Tx septic arth
Synovial lavage with balanced electrolyte solution +/_ DMSO; broad Abx (IA intermittent best concentration at synovium)
52
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
53
Hyperextension of canine limb, adduction of elbow, circumduction of distal limb with carpal flip
Infraspinatus contracture from fibrosis in working dogs
54
Infraspinatus contrcture tx
infraspinatus tenotomy- cut infraspin tendon
55
Scapulohumeral luxations- types, which more common
Medial (smaller dogs, congenital), lateral (larger dogs, less common)
56
Scap-hum lux- medial - sx types, which better
Open or closed reduction, open better, closed re-lux
57
What makes tx for Scap-hum luxation successful
Normal anatomy of glenoid still viable- if not, must arthrodese joint
58
Open scap-hum- medial: reduction- method
Use biceps brachii tendon as support to replace ruined collateral ligaments
59
Bandage for scap-hum sx
Spica
60
Scap-hum lux- Lateral: Sx
Closed with spica possible, open same as medial (biceps brachii tendon replacing lateral collaterals)
61
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)
62
Tx bicipital tenosynovitis
1-2 steroid inj into tendon within joint, if returns, transect tendon at attachment- Popeye procedure
63
Dx bicipital tenosynovitis
U/S helpful for fluid pockets, etc; Pain on direct pressure to tendon while flex shoulder, extend elbow
64
What way do traumatic elbow luxations occur
R and U go laterally to humeral condyle bc trochlea more distal than capitulum
65
Dx traumatic elbow luxations
Rads- orthogonal view, bc easy to miss on lateral!!!
66
Tx traumatic elbow luxations
REDUCE ASAP, closed preferred
67
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)
68
Congenital elbow lux- signalment
Small breed and bulldogs
69
Tx Congenital elbow lux
early sx
70
Angular limb deformity- etiology, location
Premature closure of GP in antebrachium; distal ulnar physis, gives radius curvus due to tethering of paired bones
71
What must you do in elbow trauma of
Document want owner back in 3 weeks for rads to ensure no GP damage
72
Canine carpal hyperextension injury- etiology
Large, working- trauma > degen, tear carpal ligaments (palmar fibrocartilage plate)
73
tx Canine carpal hyperextension
COAPTATION WONT WORK- pancarpal arthrodesis needed in 90%
74
Most common sites of OCD
Caudal humeral head! humeral condyle, lateral femoral condyle, talus
75
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
76
OCD-
Sequelae to OC, crack present, communicates with joint
77
Signs of OC/OCD on rads
OC- flattened/concave subchon bone; OCD- no different, flap cant be seen! soft tissue opacity
78
OC- tx
NOTHING
79
OCD progression- where is lameness most often
Shoulder or elbow
80
Dx OCD in shoulder
Pain on flexion and extension
81
Tx OCD
Remove the flap- arthroscopy preferred
82
Elbow dysplasia conditions
UAP, OC/OCD of hum condyle, FCP
83
Elbow dysplasia from FCP- signalment
Rottweiler
84
UAP- describe
Failure of fusion of anconeal process to olecranon
85
UAP- dx
Extended and FLEXED view of elbow to see anc proc within hum condyle
86
UAP- signalment
males, GSD or basetts
87
UAP- causes
R/U incongruity- ulna too short
88
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
89
OCD of humeral condyl- location, signalment
Medial, chocolate labs
90
Dx humeral condyle OCD
Cranio-lateral, Caudo-medial oblique rads (with lateral, CC, flexed)
91
Most common elbow dysplasia disease
FCP
92
FCP etiology
RARELY traumatic- usually repetitive cyclic loading- ulna narrow concavity, step from short radius
93
FCP- dx
Biggest clue: DJD of medial elbow compartment (rads not great but lateral view- secondary DJD changes in absence of UAP or OCD
94
Inherited elbow dysplasia conditions-
FCP and OCD
95
Panosteitis- signalment, findings
young, large, growing dogs; palpation painful at metaph/diaph region
96
Panosteitis- CS
Shifting lameness, SYSTEMIC SIGNS
97
Panosteitis- describe, dx
hypervascular response in medullary a/v, Rads: increased opacity on rads; IDIOPATHIC, SELF RESOLVING
98
Define hip dysplasia
Abnormal development (often too fast) of CF joint causing laxity and leading to OA (
99
Hip dysplasia key initial feature
Joint laxity before CS from OA
100
Hip dysplasia - dx
Ortolani test
101
OFA vs PennHip
OFA subj/min 2yr, Penn- obj, any age
102
TPO- parts
Ilium, ischium, pubis
103
Juvenile symphysiodesis
Improve acetabular coverage dorsally via premature closure of GP
104
Hip dysp goals
Young- prevent DJD, elim pain; Old- elimin OA pain
105
Three major stabilizers of hip
Round ligament, joint capsule, dorsal acetabular rim geometry
106
Traumatic hip lux- classification
Craniodorsal (SOME ventral)
107
Dx hip lux
CrDorsal- needs two views to diff'ate lux from sublux, underlying dysplasia
108
Best Tx hip lux
Toggle pin
109
Primary restraints- stifle
Cr and Ca cruciates, Mand L collaterals
110
Cr Cruciate job
Prevent displacement of tibia cranial to femur
111
Chronic CCL degen rupture- cause
Chronic repetitive fatigue of ligament
112
Concurrent injury with CCL
Medial meniscus- CAUDAL HORN crushed by femoral condyle sublux
113
Dx CCL rupture on rads
JOINT EFFUSION (no longer fat opacity)
114
Patellar lux grades
IN/IN, IN/OUT, Out/In, out/out
115
Tibial osteotomy- result
For CCL rupture, neutralize tibial thrust
116
TPLO-
MOST COMMON CCLr, reduced angulation of plateau
117
Most common patellar lux-
Medial, small dogs
118
Sx for patellar lux IF
CS at home
119
Trochlear wedge recession
Remove osteochondral block, then replace after removing bone underneath- for patellar lux
120
Patellar sx options (2)
Tighten laterally or release medially
121
OCD hindlimb- locations
Lat fem cond, medial troch ridge of tallus (STILL MORE COMMON IN FORELIMB)
122
Tx- OCD hindlimb
Flap excision > conservative mgmt
123
Hip dysplasia sx indications
Young:: TPO, JPS; Old: FHO (salvage), total hip
