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259 Cards in this Set
- Front
- Back
what disease is associated with intramedullary sclerosis?
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panosteitis
|
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how does panosteitis present radiographically?
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intramedullary sclerosis, especially in the appendicular skeleton
|
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after a bone insult occurs, how long does it take for:
- periosteal reactions to occur? - bone lysis to occur? |
- periosteal reactions: 10-14 days
- bone lysis 3-5 days |
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what are three basic categories of periosteal reactions, as they appear radiographically?
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1. solid
2. lamellar (onion skin) 3. interrupted |
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what are two radiographic presentations for solid periosteal reactions?
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1. smooth
2. irregular |
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what are three radiographic presentations for interrupted periosteal reactions (in order of increasing aggressiveness)?
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1. spiculated
2. sunburst 3. amorphous |
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what are two subjective assessments of the zone of transition in a bone reaction and what do they tell you about the pathologic process?
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1. length: the longer the zone of transition, the more aggressive the lesion
2. margins: well-defined margins are inactive; poorly-defined margins are active |
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pathologic new bone formation at the origin or insertion (to a bone) of a tendon, ligament, or joint capsule
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enthesophyte
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what is an enthesophyte?
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pathologic new bone formation at the origin or insertion (to a bone) of a tendon, ligament, or joint capsule
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what are the three most common radiographic signs of DJD? What are five other less common findings?
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1. intracapsular soft tissue swelling
2. osteophytes at the perichondral margin of the joint ("bone spur"/lipping) 3. enthesophytes - others - 1. joint mice 2. sub-chondral bone sclerosis 3. sub-chondral bone cyst - even less common - 4. decreased joint space (when weight bearing) 5. sub-chondral bone erosions (more common in LA) |
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what is the pathologic process of osteophyte formation?
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articular cartilage proliferation in non-weight bearing areas of joint → outgrows nutrient supply and dies → invaded with BV → replaced with bone
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what are the two most common locations of osteophyte formation in DJD of the shoulder?
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1. caudal to the infraglenoid tubercle
2. caudal to the humeral head |
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what are the six physes of the shoulder and elbow joints?
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1. supraglenoid tubercle
2. head of the humerus 3. distal humerus 4. anconeal process of the ulna 5. olecranon process of the ulna 6. proximal radius (neck) |
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where are the three most common sites of osteophyte formation in DJD of the elbow joint? What are two other less common places that appear in more severe disease?
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1. the anconeal process of the ulna
2. the head of the radius 3. the medial coronoid process of the ulna 4. the lateral aspect of the distal humeral condyle 5. the medial trochlea of the humerus |
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what is a common radiographic prognostic sign of early canine hip dysplasia?
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the Morgan line, a curved enthesophyte on the distal neck of the femoral neck
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in a normal canine coxofemoral joint, how much of the acetabular rim should overlap the femoral head?
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at least 50%
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in DJD of the stifle, what are two signs of intracapsular soft tissue swelling? What are two common places of osteophyte formation?
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- ICST swelling: cranial displacement of the infrapatellar fat pad and obliteration of the caudal fascial stripe sign
- osteophytes on the patella and the medial trochlear ridge of the femur |
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what usually causes enthesophytes?
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they occur secondarily to chronic strain, trauma, or previous avulsion at the site
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what happens to the femoral neck in hip dysplasia?
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it thickens
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what are four diseases that can cause intracapsular mineral bodies in the appendicular skeleton?
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1. avulsion fragment
2. OCD (joint mouse) 3. synovial osteochondroma 4. chondrocalcinosis |
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rounded mineral bodies in the joint caused by metaplasia and mineralization of synovial membrane
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synovial osteochondroma
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what are nine general radiographic signs of DJD
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1. intracapsular soft tissue swelling
2. joint space alterations 3. periarticular new bone (osteophytes) 4. perichondral new bone (osteophytes) 5. subchondral osteosclerosis 6. soft tissue mineralization 7. subchondral osteolysis 8. subchondral bone cyst 9. joint mice |
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what causes a decrease in the width of joint space in DJD?
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destruction of the articular cartilage
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what causes an increase in the width of joint space in DJD?
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acute and sever inflammation due to synovial effusion
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what causes periarticular new bone formation in DJD?
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excessive buildup of cartilage outgrows the ability of the synovial fluid to nourish it. It dies and mineralizes in non-weight bearing areas of the joint to attempt to stabilize the joint.
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in DJD, where does perichondral new bone form?
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at the chondro-synovial junction, fibrocartilage elements form and mineralize into osteophytes
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what is the etiopathogenesis of subchondral osteosclerosis in DJD?
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usually caused by bone-on-bone contact in weight-bearing joints due to the loss of articular cartilage, sclerosis is formed by hypertrophy of the trabecular bone to compensate for the increased weight-bearing requirement of the bone
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what are four important pieces of information to take in the history for an orthopedic exam?
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1. chief complaint
2. manner of onset (acute < 10d, chronic) 3. signs seen by the owner 4. duration of signs |
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what percentage weight does a dog bear on its forelimbs?
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60%
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what are varus and valgus?
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- varus = "bow-legged"; a deformity of the limbs toward the midline
- valgus = deformity of the limbs away from midline (e.g. the front legs of a Basset hound) |
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what are three important muscle masses to palpate when examining a dog for lameness?
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- mm of the spine of the scapula
- mm in relation to the greater trochanter - quadriceps |
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what are five characterizations that should be used to describe the specifics of a lameness in the dog?
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1. weight-bearing vs. non weight-bearing
2. neurologic or orthopedic 3. appendicular or axial 4. bone vs. soft tissue injury 5. specific joint vs. multiple joint involvement |
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for a forelimb lameness in a dog, what is an important neurological rule-out
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peripheral nerve sheath tumor
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what is the normal sitting posture of a dog that is not lame?
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the tuber ischii rests on the tuber calcanei
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characterize a Grade 1 lameness and a grade 4 lameness in the dog (1-4 grading scale)
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- Grade 1: 75% weight-bearing
- Grade 4: non weight-bearing |
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when a dog is lame in the front, when in motion, how does head position correlate to lameness?
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the head goes down on the sound limb; the head goes up when weight is baring on the lame leg to shift weight away from that limb
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what two techniques are used to assess a cranial cruciate tear in a dog?
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tibial compression and cranial drawer
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what test is used in a specific orthopedic of the exam of the dog to check for hip laxity / hip dysplasia?
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Ortolani test
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what is an Ortolani sign
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a click or pop, representing a subluxation of the coxofemoral joint when performing a Ortolani test for hip laxity / hip dysplasia on a dog
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what considerations should be made when performing an Ortolani test on a young dog
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young dogs naturally have some laxity in their coxofemoral joints
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what are four procedures commonly performed on a dog during a sedated orthopedic examination?
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1. repeating of specific portion of orthopedic exam
2. radiographic assessment 3. joint tap 4. biopsy |
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what are the three basic types of joints?
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1. fibrous joints
2. cartilaginous joints 3. synovial joints |
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what type of cartilage is load-bearing
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hyaline cartilage
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what comprises the joint capsule?
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- outer layer made of fibrous connective tissue
- inner layer with a thin subsynovium and a synovium, the latter being in contact with the synovial fluid - nerves, BVs, and lymphatics interposed between the synovial membranes and the fibrous capsule |
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what are the types of synovial cells and their functions?
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- Synovial A cells: primarily phagocytic; secrete IL-1 and PGE
- Synovial B cells: fibroblast-like; primarily secretory; secrete hyaluronan |
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what are three types of fibrous joints (and an example of each)?
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1. syndesmosis (temporohyoid joint)
2. suture (skull) 3. gomphosis (tooth sockets) |
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what are two types of cartilaginous joints (and an example of each)?
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1. hyaline cartilage / synchondrosis (growth plates)
2. fibrocartilage / amphiarthrosis (mandibular symphysis) |
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what are components of normal synovial joint fluid?
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- mononuclear cells (synovial cells, monocytes, lymphocytes, PMNs)
- ultrafiltrate of plasma - secretions of synovial B cells (e.g. hyaluronic acid) |
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what are the three basic functions of synovial fluid?
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1. lubricate the joint
2. stabilize the joint (shear stress, energy absorption) 3. nutrition (articular cartilage, intra-articular ligaments) |
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what percentage of hyaline cartilage is ECM and what is the rest?
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90% extracellular matrix; 10% chondrocytes
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what comprises the extracellular matrix of hyaline cartilage?
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- water (> 70%)
- collagen - non-collagenous proteins - enzymes - proteoglycans |
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proteins in the articular cartilage collagen matrix:
- structure - composition - basic function |
- high MW brush polymer (and the side chains are brushes)
- core: hyaluronate polymer (a glycosaminoglycan) with aggrecan (a proteoglycan) side-chains - side-chains: aggrecan (chondroitin sulfate and keratin brushes on a link protein, which serves as core polymer) - the brushes are negatively charged to provide rigidity to the chain; the polymer itself provides resilience and flexibility to the collagen connective tissue matrix |
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explain how proteoglycans, collagen, and water form a viscoelastic articular cartilage
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- collagen forms the matrix
- proteoglycans are locked into place by the collagen and form aggregates with hyaluronan - proteoglycans resist deformation, hold water, and control the transport of molecules and ions - water flows in and out of the semi-permeable cartilage and gives it the viscoelastic property |
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hyaluronan:
- type of molecule - typical concentration in synovial fluid - function |
- a non-sulfated glycosaminoglycan (high MW amino polysaccharide)
- 0.1 - 5 mg/ml - provides lubrication as well as nutrition to the joints; gives high viscosity to synovial fluid |
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what advantage does high viscosity give to a synovial joint?
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- supports transient shear stress
- absorbs some energy generated by movement - boundary lubrication |
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what are the zones of articular cartilage?
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- synovial fluid
1. zone 1 - superficial/tangential zone 2. zone 2 - transitional zone 3. zone 3 - radial zone 4. tide mark 5. zone 4 - zone of calcified cartilage |
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zone 1 of articular cartilage:
- name - structure - function |
- superficial / tangential zone
- small, flat chondrocytes and collagen fibrils that line up parallel with the articular surface - withstands SHEAR STRESS (tension in the plane of the articular surface) |
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zone 2 of articular cartilage:
- name - structure - function |
- transitional zone
- spherical chondrocytes with large collagen fibrils arranged in an intricate 3D matrix - increased resilience to COMPRESSIVE LOADING |
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zone 3 of articular cartilage:
- name - structure - function |
- radial zone / deep zone
- largest zone; chondrocytes arranged in short columns perpendicular to the joint surface; highest proteoglycan and least water; more rigid matrix that may have partially calcified cartilage (hydroxyapatite crystals) - increased resilience to compressive loading |
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zone 4 of articular cartilage:
- structure - function |
- zone of calcified cartilage
- separated from the preceding zones by the tidemark - anchors the articular cartilage to the subchondral bone |
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meniscus
'- composition - seven major functions |
- composition of fibrocartilage
1. distribution of joint fluid (lubrication) 2. shock absorption 3. load bearing 4. joint congruency 5. stabilization of joint 6. proprioception 7. prevent synovial entrapment |
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what is the term used to describe the reduction of friction in a joint by exudation of fluid from articular cartilage?
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weeping lubrication
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ability of joint fluid to change its viscosity based on movement of the joint
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thixotropy
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in articular cartilage, how is load resisted (energy dissipated) by:
- collagen fibrils? - proteoglycans? |
- collagen: tensile strength
- proteoglycans: compression resistance |
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what are three responses of articular cartilage, when put under a load, that facilitate the structural stability and mobility of the joint?
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1. they increase contact area (distributes the load)
2. increase joint conformity (stability) 3. exudes a thin gel of concentrated lubricant between the articular surfaces |
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subchondral bone:
- composition - function |
- mixture of trabecular and compact bone
- gives structural support to the overlying articular cartilage |
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what is the response of subchondral bone during loading and how does confer stability to the joint?
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- it bends
- it keeps congruent contact of joint surfaces - stress dissipation across the joint |
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what are three common contributors to abnormal joint motion?
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1. ligament rupture
2. developmental or anatomic abnormalities 3. abnormal physiologic loads on cartilage |
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what are three negative consequences of abnormal physiologic loads on articular cartilage?
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1. fracturing or fissuring of the cartilage matrix
2. disruption of the collagen fibril network 3. cell death |
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Why is rigid internal fixation necessary for fractures involving the articular cartilage?
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- the reduction of the fracture needs to be as close to the original anatomy as possible
- as such, rigid stabilization is needed during the healing process |
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What is the difference in healing between superficial cartilage defects and full thickness cartilage defects?
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- superficial defects (that do not extend to the bone) do not elicit an inflammatory response and heal by chondrocyte proliferation and new matrix production
- full thickness defects (those that extend to the subchondral bone) elicit an inflammatory response, which produces fibrin and collagen; the defect fills with fibrocartilage |
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inflammation of the biceps tendon and surrounding sheath
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bicipital tenosynovitis
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what are two radiographic signs for bicipital tenosynovitis in the dog?
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1. intertubercular groove sclerosis
2. bicipital tendon mineralization |
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what is the end stage of septic arthritis?
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subchondral bone lysis
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what is the most common etiology for septic arthritis?
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bacterial infection
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what type of septic arthritis would bacteremia produce?
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septic polyarthritis
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what are two common etiologies for mono-articular septic arthritis?
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1. puncture
2. surgery |
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what are three common radiographic signs of severe septic arthritis in the stifle?
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1. IC ST swelling
2. obliteration of the caudal fascial stripe 3. lysis of bone |
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what are two radiographic signs of an aggressice joint lesion?
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1. intracapsular soft tissue swelling
2. permeative/punctate/moth-eaten lysis of multiple bones in the joint |
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what are the three components of the syndrome of erosive polyarthritis?
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1. sub-chondral erosions
2. joint subluxation 3. intracapsular soft tissue swelling |
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what is the most common site for erosive polyarthritis in the small animal and how does it appear radiographically?
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- most commonly at the distal extremity (metacarpal/metatarsal-phalangeal joints)
- whereas the articular surfaces of the metacarpal/metatarsal bones normally have a "dumbbell" appearance, in erosive polyarthritis, they have a "pencil" appearance - intracapsular soft tissue swelling (consistent with an aggressive joint lesion) |
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what are two common differentials for erosive polyarthritis?
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1. rheumatoid arthritis
2. feline non-infectious polyarthritis |
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describe the radiographic findings of erosive polyarthritis from onset and as it gets worse
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1. starts with intracapsular soft tissue swelling with no apparent bony lysis
2. incarease coarseness to the trabecular pattern of affected bones may be noted 3. lucent, cyst-like lesions in the subchondral bone at the joint capsule attachments and later on the articular margins 4. cystic lesions progress to irregular erosion of the subchondral bone and marked destruction of the joint surface 5. subluxation and luxation of joints due to destruction of the ligaments |
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what are the radiographic characteristics of non-erosive polyarthritis?
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- normal bone
- intracapsular soft tissue swelling - polyarticular (may be nonoarticular early) |
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what are the most common joints for non-erosive polyarthritis?
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tarsus, carpus, stifle
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what is the main differential for non-erosive polyarthritis?
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lupus
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what are six locations for joint associated tumors from most common to least common?
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1. stifle (most common)
2. elbow 3. shoulder 4. carpus 5. tarsus 6. hip (less common) |
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what are four differentials for joint associated tumors?
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synovial cell sarcoma, histiocytic sarcoma, synovial myxoma, undifferentiated sarcomas
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what is a common sequela to a joint associated tumor of the stifle
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cranial cruciate ligament tear
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a lesion appearing similar to erosive polyarthritis, but only of a single joint is likely what?
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joint associated tumor (synovial cell sarcoma)
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describe the radiographic signs of a joint associated tumor
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1. severe, lobulated intracapsular soft tissue swelling
2. lysis of bones in the joint |
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what are two differentials for MONOarticular intracapsular soft tissue swelling WITHOUT bone lysis
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1. effusion (DJD, trauma, hemarthrosis, etc.)
2. synovitis |
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what are two differentials for MONOarticular intracapsular soft tissue swelling WITH bone lysis
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1. septic arthritis
2. joint associated tumor |
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what are two differentials for POLYarticular intracapsular soft tissue swelling WITHOUT bone lysis
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1. effusion (DJD, hemarthrosis, etc.)
2. non-erosive polyarthritis |
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what are two differentials for POLYarticular intracapsular soft tissue swelling WITH bone lysis
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1. erosive polyarthritis (most common SA)
2. septic arthritis (most common LA) |
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what are three signs that define the syndrome of osteoarthritis?
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1. articular cartilage degeneration
2. marginal bone hypertrophy 3. synovial membrane changes |
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what are two common synonyms for osteoarthritis?
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DJD, osteoarthrosis
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what is the end stage of osteoarthritis?
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ankylosis
|
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what are the two basic types of osteoarthritis?
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primary (unknown cause, rare) and secondary (known cause, most common)
|
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what are five causes of secondary osteoarthritis?
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1. previous trauma
2. joint instability 3. inflammation 4. developmental conditions 5. joint incongruency |
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what are the two basic physiological abnormalities that can lead to cartilage breakdown and osteoarthritis?
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1. abnormal stresses on the cartilage
2. abnormal cartilage |
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what are five causes of abnormal stress that can lead to failure of normal articular cartilage?
|
1. developmental/anatomic abnormalities
2. obesity 3. microfractures and bone remodeling 4. trauma 5. loss of joint stability |
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what are five causes of abnormal articular cartilage that will fail under normal stress?
|
1. genetic and metabolic disease
2. aging 3. administration of toxins (e.g. enrofloxacin) 4. inflammation 5. immune responses |
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in osteoarthritis, what pathophysiologic changes are caused by cartilage fibrillation/fissuring?
|
- cellular alteration
- release of inflammatory mediators |
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when cartilage is damaged in osteoarthritis, how does it change on the molecular level?
|
degradation of collagen and proteoglycan
|
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describe the pathogenesis of how an abnormal stress on articular cartilage leads to pain and lameness in osteoarthritis
|
abnormal stress → collagen and proteoglycan destruction → loss of matrix components and decreased cartilage synthesis → breakdown of articular cartilage → pain and lameness
|
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describe the two basic theories of why cartilage breaks down under stress overload.
|
-Theory A: (physiologic) cell injury leads to a degradative response, releasing enzymes that degrade cartilage
-Theory B: (mechanical) a biomaterial failure leads to mechanical failure of the collagen network and unravelling of proteoglycan |
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what are seven (variable) clinical signs of osteoarthritis?
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1. stiffness
2. exercise intolerance 3. lethargy 4. joint effusion 5. lameness 6. pain 7. disuse atrophy |
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what are four common clinical findings of osteoarthritis on physical examination?
|
1. decreased joint range of motion
2. crepitus 3. muscle atrophy 4. muscle asymmetry |
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what are six common radiographic findings for osteoarthritis?
|
1. osteophytes and enthesiophytes
2. joint effusion 3. subchondral bone sclerosis 4. bone remodeling 5. thickening of periarticular soft tissues 6. cartilage destruction |
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what are the five basic principles of treatment of joint disease?
|
1. weight management
2. nutritional supplementation 3. exercise moderation 4. physical rehab 5. NSAIDs and other medical therapies |
|
what is the most common nutritional supplement for osteoarthritis? How does this work?
|
ω-3 fatty acids decrease the amount of arachidonic acid in the cell membranes and therefore decrease the production of COX/lipoxygenase inflammatory mediators
|
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what is a DMOA (with regards to nutritional supplements)
|
"disease modifying osteoarthritic agent"; a chondroprotective nutritonal supplelement
|
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what are four proposed mechanisms by which chondroprotectives/DMOA supplementation is said to provide their beneficial effects?
|
1. promote cartilage matrix synthesis
2. slow cartilage degradation 3. decrease breakdown products 4. anti-inflammatory effects |
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name five different chondroprotectives for joint disease
|
1. chondoitin sulfate
2. Polysulfated glycosaminoglycans 3. hyaluronic acid 4. mangnese 5. vitamin C |
|
what is a possible complication of PSGAG (polysulfated glycosaminoglycans)
|
they have heparin-like activity and can cause thrombocytopenia
|
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in treating joint disease, what does the term "controlled exercise" mean?
|
rehabilitation to correct abnormalities with gradual introduction and consistent activity. Inactivity and extreme activity may worsen the situation.
|
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in the treatment of joint disease, what are five goals of physical rehabilitation therapy?
|
1. increase strength and endurance
2. increase joint ROM 3. decrease edema 4. promote tissue repair/metabolism 5. decrease muscle spasms and pain |
|
what are four severe complications of NSAID administration?
|
1. GI ulcers/upset
2. nephrotoxicity 3. hepatotoxicity (carprofen; especially in labradors) 4. keratoconjunctivitis siccs (etodolac) |
|
what are three commonly prescribed COX-2 NSAIDs for treatment of joint disease?
|
1. carprofen
2. meloxicam 3. deracoxib |
|
what are five contraindications for the use of NSAIDs in the treatment of joint disease?
|
1. renal disease
2. gastric ulcers 3. bleeding disorder 4. hepatic disease 5. if patient is on a corticosteroid |
|
what type of analgesic should ntop be combined with NSAIDs
|
corticosteroids
|
|
name four analgesics that can be combined with NSAIDs in the treatment of joint disease and what class of drugs they are.
|
1. tramadol - an opiate
2. gabapentin - Ca channel blocker 3. amantadine - NMDA receptor antagonist 4. amitriptyline - tricyclic antidepressant |
|
what are four basic types of medical magament techniques to treat septic arthritis (in order of least sever to most severe cases)
|
1. antimicrobials
2. surgical/arthroscopic lavage 3. drain placement 4. open joint management |
|
what is the proper method of using antimicrobials to treat septic arthritis?
|
- give antibiotic immediately after joint fluid samples are taken
- alter the antibiotic based on culture/susceptibility testing - treat 4-6 weeks; continue 2 weeks after resolution of clinical signs |
|
what drugs are commonly used to treat (sterile) non-erosive polyarthritis?
|
-corticosteroids such as prednisone
- immunosuppressives (azathioprine, cyclosporine, cyclophosphamide) |
|
what are two common treatments for rheumatoid arthritis?
|
1. immunosuppressive drugs
2. arthrodesis (surgical joint immobilization) |
|
what distinguishes calcified cartilage from hyaline cartilage?
|
- matrix calcified and is invaded by blood vessels
- osteoid is produced, scaffold for bone formation |
|
before skeletal maturity, and during growth, what must be true of cartilage production and bone replacement?
|
they must be equal so that the growth plate is maintained
|
|
what is the term for the tissue supplied by blood vessels to cartilage during endochondral ossification?
|
osteogenic granulation tissue
|
|
what is the most common site for OCD? What other two places is OCD less commonly found?
|
- most common: articular-epiphyseal complex
less common: metaphyseal and apophyseal growth plates |
|
what is the basic process of endochondral calcification?
|
orderly calcification of cartilage matrix → vascular invasion → deposition of osteogenic granulation tissue → replacement of cartilage by bone tissue
|
|
define OCD in one sentence
|
A developmental orthopedic disease, caused by the disruption of endochondral ossification, characterized by a focal area of developing cartilage at the osteochondral junction that fails to calcify and instead thickens and degenerates.
|
|
what are the two basic processes of endochondral ossification that DON'T happen, that leads to OCD?
|
- failure of matrix calcification
- lack of vascular ingrowth |
|
why do areas of cartilage in OCD become necrotic?
|
because the thickened cartilage has poor diffusion of nutrients from synovial fluid
|
|
since in OCD, there is a failure of calcification and vascular invasion, what type of cartilage does the OCD lesion represent?
|
it becomes more like articular cartilage, as opposed to calcified cartilage that will turn into bone
|
|
separation between calcified and non-calcified layers of joint cartilage
|
tidemark
|
|
in OCD, at what location does the fissure develop that breaks off into a flap?
|
at the tidemark
|
|
what are the three fates of a cartilage lesion in OCD?
|
1. reattachment (very rare)
2. vertical fracture of articular cartilage may form 3. detachments of fragments, which become joint mice |
|
theoretically, how could a cartilage flap reattach to subchondral bone?
|
a bleeding defect beings in mesenchymal cells
|
|
in OCD, why might a vertical fracture of articular cartilage form? What are clinical signs associated with this? Why will this fracture not heal?
|
- fracture caused by motion of flap against the cartilage during weight-bearing motion
- irritation causes synovitis, pain, lameness, and OA - the fracture does not heal because of the synovial fluid interposed in the fracture |
|
in OCD, why is a joint mouse often larger than the lesion from whence it came?
|
the cartilage flap was not dead when it broke off; it continued to enlarge due to nutrition from synovial fluid
|
|
what are six basic etiologic factors leading to OCD?
|
1. trauma
2. anatomical factors 3. hormonal factors 4. heredity (familial, breed predisposition) 5. over nutrition (especially excess dietary Calcium) 6. rapid growth rates |
|
how does trauma contribute to the development of OCD?
|
- while ischemia of subchondral bone has been shown as a cause in humans, it does not appear to be a cause in dogs
- biomechanical stress (repeated microtrauma) most likely the cause of flap formation |
|
how do anatomical factors of contribute to OCD in the canine humeral head?
|
the cartilage is particularly thick in this location. Since the caudomedial aspect of this cartilage develops more slowly, it is susceptible to microtrauma from the glenoid
|
|
how do hormonal factors contribute to OCD?
|
- excess growth hormones (particularly somatotropin and thyrotropin) contribute to thickening of the cartilage
- testosterone (esp. in males) is synergistic with growth hormones and delays endochondral ossification - in contrast, estrogen encourages cartilage calcification |
|
why are males overrepresented for OCD?
|
because testosterone promotes growth of cartilage and delays endochondral ossification, whereas estrogen encourages cartilage calcification
|
|
what dog breed and breed-types are most susceptible to OCD?
|
Great Danes, St. Bernards, Labradors, Rottweilers, and other large and giant breeds, especially those with adult weights > 20kg
|
|
in which species does ischemia a cause of OCD and why does this lead to OCD? What is the proposed reason why ischemia occurs?
|
- pigs, horses, humans
- leads to cartilage necrosis - may be related to rapid growth rate |
|
for suspected OCD, why should you always radiograph both joints?
|
because OCD is very often bilateral, although lameness may appear to be only on one limb.
|
|
where are the four most common sites of OCD in the dog, and what is the prognosis for lameness after medical and/or surgical intervention?
|
1. shoulder - good (75%)
2. elbow - guarded 3. stifle - guarded 4. hock - poor |
|
what is the common site of OCD in the shoulder?
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caudal aspect of the humeral head
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what is the common site of OCD in the elbow?
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distal trochlear ridge of the medial aspect of the humeral condyle
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what is the common site of OCD in the stifle?
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medial aspect of the lateral femoral condyle
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what is the common site of OCD in the hock?
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usually on the plantar aspect of the medial trochlear ridge of the talus
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comment on the incidence (male:female and how often bilateral) in OCD of the
- shoulder - elbow - stifle - hock |
- shoulder: males 2:1-6:1; 20-85% bilateral
- elbow: males 2:1; 20-50% bilateral - stifle: males 3:1; 72% bilateral - hock: males=females; 40% bilateral |
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what two dog breeds are overrepresented for OCD of the hock?
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Rottweilers and Labradors
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what is a DMOA?
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disease modifying osteoarthritic agent
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generally, when is medical management preferred over surgery for treatment of OCD?
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- young age (< 7 months old)
- in OCD of the hock, older dogs with sever OCD (due to poor prognosis of surgery) - small radiographic lesions - no joint mice - no clinical pain |
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generally, when is surgical treatment indicated for OCD?
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- > 8 months of age
- flap/joint mouse present - persistent lameness (> 6 weeks) - large lesion |
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what are four aspects for conservative medical treatment of OCD?
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1. strict cage rest for 4-6 weeks
2. NSAIDs 3. DMOA supplementation (disease modifying osteoarthritic agents) 4. restricted diet (calories and calcium) |
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In mild-moderate cases of OCD, why is it sometimes preferable to just go ahead and do surgery instead of trying to manage it conservatively?
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because it has been shown that surgery allows more rapid return to function and minimizes the development of OA
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what are the three basic aims of surgery to treat OCD?
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1. remove flap/joint mice
2. remove non-adherent cartilage in the periphery of the lesion 3. stimulate the defect to heal by fibrocartilage formation (curettage, forage, abrasion arthroplasty) |
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what are the two basic surgical approaches to treat OCD?
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1. arthrotomy
2. arthroscopy |
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with regards to OCD, what is the OATS surgical procedure?
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- osteochondral autograft transfer system
- transfer articular cartilage and subchondral bone from one site in the body to the other in the same patient |
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what are four complications of joint surgery?
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1. seroma
2. wound dehiscence 3. infection 4. chronic lameness |
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what are the three basic radiographic findings of an osteochondritic lesion?
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1. intracapsular soft tissue swelling
2. subchondral defect/flattening of articular surface 3. sclerosis surrounding the OC lesion |
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why might a flap from OCD not be seen on a radiograph
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because to be seen it requires mineralization; cartilage silhouettes with other soft tissue
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what is the average age range of osteochondrosis in dogs
- in the shoulder? - in the stifle? - in the elbow? - in the hock? |
- shoulder: 6-9 months
- stifle: 6-10 months - elbow: 6-8 months - hock: 6-12 months |
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when performing radiography on a shoulder for osteochondrosis, and it appears unilateral, what should you do to make sure it is only unilateral?
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perform a rotated limb view to expose more of the caudal humeral head
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what view is best to radiographically visualize OCD of the shoulder?
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lateral or rotated lateral
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what views are best to radiographically view OCD of the stifle?
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lateral and cranial-caudal
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what normal anatomic feature of the stifle can be confused for osteochondrosis?
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the extensor fossa on the lateral femoral condyle
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what views are best to radiographically view OCD of the hock?
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cranial-caudal; lateral; and oblique for the lateral trochlear ridge (due to superimposition of the talus)
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where is intracapsular soft tissue swelling usually seen radiographically in the hock of the young dog that may lead you to suspect osteochondrosis?
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on a lateral view:
- dorsal to the calcaneus/caudal to the tibia - dorsal to the trochlea of the talus/cranial to the tibia |
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what are four conditions that encompass the term "elbow dysplasia"?
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1. ununited anconeal process
2. fragmented medial coronoid process (of the ulna) 3. osteochondrosis 4. premature radius/ulna physis closure |
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what view is best to radiographically view osteochondrosis of the elbow?
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cranial-caudal projection is the only good view
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what radiographic view is best to visualize an ununited anconeal process?
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flexed lateral
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anconeal process:
- when should it unite with the ulna? - if ununited, is this most often a unilateral or bilateral condition? - what breed of dog is predisposed to this condition? |
- should unite by 5 months of age
- often bilateral - German Shepherd Dog |
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what is the best method to visualize a fragmented medial coronoid process of the ulna?
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CT
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what is the most common developmental elbow disorder?
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fragmented medial coronoid process
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radiographically, besides the primary lesion, what other lesions are associated with a fragmented medial coronoid process of the ulna?
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- osteophytes on the anconeal process and radial head
- sclerosis of the trochlear notch of the proximal ulna |
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how does growth of the ulna compare to that of the radius?
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the ulna has only one physis (distal to the elbow) whereas the radius has two physes; so the growth from one physis must equal the growth of the other two
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what are three results of a premature ulnar physis closure?
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1. lateral deviation and rotation of the manus (valgus)
2. radius curvus 3. humeroulnar subluxation |
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what is a common procedure to prevent limb deformity in the case of a premature ulnar physis closure?
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ulnar ostectomy
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what condition of the proximal radioulnar joint can cause elbow dysplasia?
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a step misalignment of the radial head and the medial coronoid process of the ulna
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what is the usual end result of a premature radial physis closure?
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humeroradial subluxation
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signalment for panosteitis:
- age - dog breeds and breed types - sex |
- most common 5-18 months, but can be seen in middle-aged dogs
- medium to large breeds; German Shepherd Dogs and Basset Hounds - male > female |
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what are two early radiographic signs of panosteitis?
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- increased medullary opacity, usually seen in the distal diaphysis of the femur near the nutrient foramen
- blurring of the trabecular pattern |
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what are two radiographic signs of advanced panosteitis
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- patchy, delineated medullary opacities
- solid (smooth/lamellar) periosteal reaction on the adjacent cortex |
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signalment for HOD:
- age - dog breeds and breed types - sex |
- 3-5 months
- Weimaraner and Great Dane; other large, rapidly-growing dogs - males > females |
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what are the most commonly affected bones in HOD?
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radius, ulna, and tibia
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what are three radiographic signs of HOD?
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1. soft tissue swelling adjacent to physis
2. linear, irregular lysis adjacent and parallel to the physis that gives the appearance of a "double physeal line" - marked metaphyseal periosteal reaction due to sub-periosteal hemorrhage |
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a form of osteochondrosis that results from temporary inadequate blood supply to the metaphysis
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retained cartilaginous core
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viewed radiographically, a wedge or conical shape in the metaphysis of the ulna
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retained cartilaginous core
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what are three synonyms for panosteitis?
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1. eosinophilic osteomyelitis
2. eosinophilic panosteitis 3. enostitis |
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signalment for panosteitis:
- age - dog breed and breed type - sex |
- juvenile dogs
- German Shepherd Dogs, Basset Hounds, large and giant breed dogs - males > females; females @ 1st estrous cycle |
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what type of bones and what part of the bones are affected by panosteitis?
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- long bones of the appendicular sksleton
- diaphysis and metaphysis |
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what are seven etiologies proposed for panosteitis?
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1. STRESS (e.g. during 1st estrous cycle)
2. eosinophilia (rare) 3. microorganisms/viruses/parasites 4. genetic 5. allergy 6. metabolic 7. autoimmune |
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what is the pathogenesis of panosteitis?
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- loss of medullary adipose tissue, followed by fibrous proliferation, intramembranous ossification, and osteoclastic removal of trabeculae
- periosteal proliferation and cortical changes seen in more severe cases - returns to normal ~60-90 days (can last up to 190 days) |
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which part of the long bone is NOT affected by panosteitis?
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the epiphysis
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describe the lameness associated with panosteitis
- onset - severity - persistence - effect of exercise and rest - location |
- acute onset
- mild to moderate weightbearing lameness - persists 2-14 days - not influenced by exercise or rest - shifting leg lameness that usually doesn't return to the same leg |
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what five bones are most commonly affected by panosetitis in the order of prevalence?
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1. ulna (most common)
2. radius 3. humerus 4. femur 5. tibia |
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what are some signs from the patient's history that might point to panosteitis?
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1. listlessness
2. reluctance to move 3. lameness (acute onset) 4. anorexia 5. no concurrent HX of trauma |
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what are two clinical signs of lameness on physical examination?
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1. pain on deep palpation of bone (mild to extremely painful)
2. mild-moderate weightbearing lameness |
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what type of imaging technique would be the best for diagnosing panosteitis?
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bone scan
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what are five differentials for panosteitis?
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1. OCD
2. hip dysplasia 3. osteomyelitis 4. Nutritional secondary hyperparathyroidism 5. trauma (strain/sprain, fracture, luxation) |
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what are four ways to medically manage panosteitis?
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1. N.B. it is self-limiting
2. control pain and inflammation 3. exercise restriction 4. ± weight reduction |
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what is a common clinical sign of a retained cartilagenous core in the distal femur
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genu valgum (knees pushed together)
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a "flame" shape to the distal ulnar physis may indicate which disease?
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retained cartilaginous core
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what is a common surgical procedure to prevent/treat radius curvus in severe cases of a retained cartilagenous core in the ulna?
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ulnar ostectomy
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what are three synonyms for hypertrophis osteodystrophy?
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1. canine skeletal scruvy
2. idiopathic osteodystrophy 3. Barlow's disease |
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what are four clinical signs of HOD on PE?
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1. (per)acute mild NON-WEIGHTBEARING lameness
2. pain on palpation 3. fever > 104 °F 4. swollen/warm/painful distal limb |
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what type of bone and where specifically in the bone does HOD occur?
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the metapheal side of the active physis on a long bone
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describe the timing of pain/lameness associated with HOD
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- episodic
- symtpmatic ≈ 1 week - multiple recurrences uncommon, 1-6 weeks apart |
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name six places where HOD can occur
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1. distal radius
2. distal ulna 3. tibia 4. TMJ 5. costochondral junction 6. scapula |
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what are five proposed etiologies for HOD?
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1. abnormal vitamin C metabolism
2. excessive vitamin/mineral supplementation 3. vacciation 4. genetic 5. immune-related |
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what abnormalities can be found in the affected area of HOD?
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1. disrupted trabeculae
2. hemorrhage 3. hemosiderin deposits 4. necrotic trabeculae 5. inflammatory cells 6. resorption of trabeculae 7. neutrophilic infiltration |
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what are the characteristics of the synovial fluid with HOD?
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- ↑ volume (1-3 ml)
- transparent, straw-colored - normal viscosity - ↑PMN |
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what are three DDx for HOD?
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1. septic arthritis
2. septic physitis 3. panosteitis |
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what is a pathognomonic radiographic sign for HOD?
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a "double-physis"
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what are some clinical signs for peracute HOD?
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- more severe than normal HOD
- < 1 day of refusal to stand - dehydration - malaise - depression - severe pain on gentle palpation of swollen areas - prolonged recumbency - anorexia - hyperthermia (106 °F) |
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how is mild-moderate HOD treated?
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- medical management (not Sx)
- N.B. self-limiting disease - NSAIDs - correct diet - ± antibiotics |
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how is severe HOD treated?
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- a short course of IV short-acting corticosteroids
- supportive care |
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how is peracute HOD treated?
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- injectible corticosteroids for a few days
- IV fluids - force feeding - well padded bedding - regular turning |
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what is a more descriptive synonym of Perthes' disease
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avascular necrosis of the femoral head / neck
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what type of dogs are affected by Perthes' diesase? Name a specific breed particularly overrepresented.
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toy and miniature breed dogs. Manchester terrier.
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what are the three basic stages of Perthes' disease?
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1. ischemia (necrosis)
2. early repair stage 3. advanced repair stage |
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in Perthes' disease, what are two major effects of disruption of the blood supply? How are chondrocytes affected? How is endochondral ossification affected?
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1. empty osteocyte lacunae
2. thickening of metaphyseal trabeculae - normal chondrocytes - no effect on endochondral ossification |
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in the early repair stage of Perthes' disease, what is the major morphological change of bone?
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collapse of subchondral bone causes a flattening of the femoral head
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in the early repair stage of Perthes' disease, in what three ways does the cartilage change?
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1. clefts and fissures in the articular cartilage due to collapse of the subchondral bone
2. thickening of the articular cartilage 3. invasion of physeal cartilage with fibrovascular repair tissue |
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in the early repair stage of Perthes' diesase, what two cardiovascular effects occur?
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1. revascularization of the epiphysis
2. resorption of necrotic bone marrow debris and dead trabeculae |
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in the advanced repair stage of Perthes' disease, describe the major alterations in the joint that will lead to progressive osteoarthritis
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1. loss of normal shape of the femoral head
2. markedly thickened articular cartilage |
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in general, why are small dogs thought to be more susceptible to Perthes' disease than larger dogs?
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because they have a more superficial blood supply, which can more easily be interrupted
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describe the arterial anatomy of the femoral head
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The lateral circumflex a., medial circumflex a., and caudal gluteal a. anastamose to form a vascular ring around the femoral neck
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describe a typical HX (3 steps) that illustrates the progression of Perthes' disease
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1. slow onset weight-bearing lameness
2. worsens over 6-8 wk 3. progresses to acute lameness |
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what are five clinical signs on PE of Perthes' disease?
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1. lameness
2. pain 3. decreased ROM 4. muscle atrophy 5. crepitus |
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what are five ragiographic signs of Perthes' disease?
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1. deformity of the femoral head
2. SHORTENING or LYSIS of the femoral neck 3. focal areas of decreased bone opacity in the femoral epiphysis 4. femoral neck fracture 5. osteoarthritis (not common in a 4-5mo animal) |
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what is the most common DDx for Perthes' disease?
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medial patellar luxation
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what are three DDx for Perthes' disease?
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1. Medial patellar luxation
2. trauma (physeal, coxofemoral luxation, femoral head or neck fracture) 3. muscle strain or sprain |
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when is surgical treatment indicated for Perthes' disease?
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if radiographic changes are evident
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what are three methods for conservative treatment of Perthes' diesase?
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1. NSAIDs
2. restricted activity for 2 months in a nonweight bearing sling 3. non-weight bearing exercises such as swimming |
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what are two common surgical options to treat Perthes' disease?
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1. femoreal head and neck ostectomy
2. total hip replacement |
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what is an FHO surgery?
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femoral head and neck ostectomy
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what are some indications for FHO surgery?
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(femoral head and neck ostectomy)
'- Perthes' disease - DJD from hip dysplasia - acetabular and femoral head/neck fractures - chronic luxation of the hip - chronic osteoarthritis of any cause - when conservative treatment has failed (quality of life issue; last resort before amputation) |
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what are the two basic cuts that are made in a FHO surgery?
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1. create a fossa to expose the neck of the femur, separating it from the greater trochanter.
2. cut from the medial aspect of the greater trochanter to the lesser trochanter, including the entire neck and head in the cut. Don't cut the greater trochanter. |
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how long after FHO surgery is swimming and other exercise encouraged?
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by 2 weeks
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what are four important factors that determine the prognosis of FHO surgery?
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1. post-operative rehab
2. surgical skill 3. activity of the dog (need exercise ASAP after Sx!) 4. muscle atrophy (the more muscle, the better) |
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how can you minimize the impact of muscle atrophy on the prognosis of post-operative limb function?
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pre-operative PT to build muscle mass
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why, in a normal animals would you see a flattened region on the femoral head?
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it is the fovea capitis, the site of attachment of the round ligament of the head of the femur
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when assessing hip dysplasia, what part of the coxofemoral joint do you look at?
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the cranial 3rd of the acetabular margin
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what are the three things that you need to look at radiographically to diagnose hip dysplasia?
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1. dorsal acetabular rim coverage (≥50%)
2. congruity along the cranial 1/3rd of the joint 3. DJD |
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what are two early radiographic signs of hip dysplasia?
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1. ostephyte formation on the caudal aspect of the femoral neck (Morgan line)
2. coxofemoral hip laxity |
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what is the proper radiographic positioning for the extended standard view of the pelvis, to diagnose hip dysplasia?
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- VD view
- pull legs down and rotate legs inward - entire pelvis and both femora, though the stifle |
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what are three things to look for when evaluating whether your extended pelvic radiograph was positioned correctly?
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1. similar contour of the wings of the ilia
2. obturator foramina should be symmetrical in shape 3. the patellae should be located in the center of the femora (trochlear groove) |
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what are the two standardized tests for hip dysplasia evaluation?
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1. OFA test
2. PennHip test |
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what are three requirements for submission of a radiograph to the OFA for evaluation of hip dysplasia?
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1. extended leg VD
2. paperwork for the animal (e.g. AKC) 3. patient must be ≥2 years old |
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what are two reasons why an extended leg VD is suboptimal for evaluating hip dysplasia?
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1. twisting of the joint capsule will force the femoral head into the acetabulum, thus artificially decreasing joint space
2. muscular tension in the unsedated patient will do the same |
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what three views are required for a PennHip hip dysplasia submission?
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1. extended leg VD
2. Compressed VD 3. distraccted VD |