• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/224

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

224 Cards in this Set

  • Front
  • Back
What does lameness indicate?
Lameness is an indication of structural or functional disorder in one or more limbs. A manifestation of PAIN, that can also be associated with mechanical disorders, neurologic disorders, weaknesses or metabolic disorders.
What age group do skeletal disorders most often occur in?
Immature animals, greatest skeletal growth is b/w the 4th and 7th months (90% of longitudinal growth)
What sex does developmental disorders more commonly occur in?
Males.
What are the steps to diagnosing a lameness?
Signalment and hx
PE
Ortho exam
Additional: neuro, lab, synovial fluid, biopsy, US, etc
T/F Accurate dx of lameness requires a thorough exam of regional topographical musculoskeletal anatomy and joint kinesiology.
True
What is the first part of an ortho exam?
Visual exam.
With a head bob, the head goes ___ when the lame limb goes ___.
Up, down.
What happens to the stride on the side that is affected?
Generally shorter.
Should you use sedation on the first exam?
No, because want to localized the pain response
insular
narrow-minded

opposite: cosmopolitan
What do you evaluate with synovial fluid?
- Viscosity, volume, cellularity, culture, color and turbidity
What is arthrography?
positive or negaitve contrast materials to enhance visualization of intra-articular structures, Especially useful with the shoulder.
T/F Synovial tissue culture is more sensitive than synovial fluid culture.
True
With biopsy of bone, how many samples should you take?
Multiple samples - generally 3 in different planes
What does the use of bone scintigraphy allow you to evaluate?
The physiology or activity of the bone - see increased bone turn over before radiographic changes. Good for obscure lameness, scanning the skeleton, multifocal neoplasia and evaluation of bone activity in healing fracture/non-union.
Can scinitgraphy allow you to differentiate between benign and malignant bone dz?
No
What can ultrasound tell you?
muscle contusions, strains, fibrosis, tendon injury
What joints in arthroscopy most commonly used to evaluate?
Elbow, shoulder, stifle.
What are the advantages of arthroscopy?
Excellent visualization
Minimal joint trauma
Shorter operative time
Low patient morbidity
What is force plate analysis?
a measurment of limb weight-bearing forces for the onjective evaluation of normal and abnormal gait.
What is an arthropathy and what are the 2 different kinds and their significance?
Arthropathies are pathological alterations in one or more components of a synovial joint.
- Arthrosis: noninflammatory, primary and secondary DJD

- Arthritis: inflammatory, infectious or non infectious (erosive and non erosive)
What is the synovial joint composed of?
- Articular cartilage
- Synovial membrane
- Synovial Fluid
- Joint capsule
What is the cell type that produces matrix and is most numerous and active during chondrogenesis but decreases in number and metabolic activity with age?
Chondrocytes
What are the two cell types in the synovial membrane?
a cells: phagocytic
b cells: synthesize and secrete SF & HA
How does the synovium respond to chronic irritation?
hypertrophy and hyperplasia
Describe normal synovial fluid.
Clear, pale yellow
Usually .25-2ml/joint
low cell count (mostly mononuclear cells)
total protein slight less than plasma
viscosity proportional to content and molecular size of HA
What happens to synovial fluid with dz, generally?
increased volume, decreased viscosity, alteration in cell number and types present
What is the function of SF?
Lubrication and articular cartilage nutrition
T/F Osteoarthrosis is the final commone pathy for many dzs.
True
What is osteoarthrosis and what is it characterized by?
Chronic, progressive, noninfectious disorder of moveable joints.

Characterized by fragmentation, loss of articular cartilage, enthesophyte and marginal osteophyte formation, sclerosis or subchondral bone and periarticular soft tissue fibrosis.
T/F With osteoarthrosis, there are signficant changes to the synovial fluid?
False. Normal or near normal.
Primary (Idiopathic) DJD/Osteoarthrosis is the result of ____ (normal/abnormal) stresses on _____ (normal/abnormal) cartliage.
Normal, abnormal
Why does Primary DJD develop (Pathology)?
Normal stress on abnormal cartilage - Limited ability of cartilage to regenerate and maintain itself in the face of cumulative effects of age, wear and trauma.
What joints are most commonly affected with Primary DJD?
Hip, shoulder, elbow, stifle.
Often multiple joint affected, disease is not always clinically apparent, treat only if clinically evident.
What type of osteoarthrosis is most common (primary or secondary)?
Secondary
How does Secondary DJD come about?
Abnormal stresses on normal cartilage, where cartilage degeneration results from conditions that cause direct damage to the cartilage (injury), cause the joint to be unstable (instability), subject articular surface to abnormal biomechanical forces (incongruity)
What are some of the etiologies of secondary DJD?
Congenital: conformation abnormalities, osetochondrosis, physeal disorders, growth deformities, aseptic necrosis, inborn errors of metabolism, neoplastic arthropathies.

Acquired/Traumatic: fractures involving the joint, luxations/Sub-lux, partial or full thickness injury to articular cartilage.

Damage to supporting structures: sprains, ligamentous injuries, tendon contractures, meniscal injuries.
List the clinical signs of primary and secondary DJD.
- decrease in physical activity
- reluctance to perform previous tasks
- pain = lameness
- stiff/lame after exercise or rest
- "warm out"
- Altered behavior
What are the PE findings of DJD?
- Pain +/- crepitation w/ joint manipulation
- Decrease range of motion
- Joint effusion
- Periarticular fibrosis, deformity of joint
T/F Lab abnormalities associated with systemic dz are usually present with DJD.
False. Systemic signs are not usually present w/ DJD
SF analysis with DJD typically shows what changes?
Decreased viscosity
Increased volume
Increased numbers of mononuclear phagocytic cells
What are the therapeutic goals of DJD trt?
Alleviate discomfort
Prevent further degen of the joint
Restore the function of the joint to as close to normal as possible
What are some of the components of DJD treatment?
Rest, controlled activity, physio, weight reduction if necessary, pharmacotherapy, surgery (as a primary trt or salvage procedure)
What are some of the different pharmacotherapies used with DJD?
NSAIDS (esp Carprofen and Meloxicam)
Slow-acting Disease Modifying Osteoarthritis Agents (SADMOA) - "Chondroprotectives" eg Cosequin and Adequan
HA
Omega 3
Corticosteriods (only indicated with immune mediated DJD)
Does surgery eliminate degenerative changes already present or prevent progression of degen changes?
No.
What is osteoarthritis?
Inflammatory joint dz, inflam changes in synovial fluid and synovial membrane, accompanied by systemic signs of illness.
What is infectious arthritis and what can cause it to develop (origin)?
Joint contaminated by pathogenic organisms that may develop in a normal joint or more likely if host resistance is impaired by concurrent immunosuppressive dz or drugs.

Can be hematogenousor nonhematogenous in origin.
Describe hematogenous infectious arthritis.
Bacteremia w/ localization in one or more joints, orginating from respiratory, digestive, urinary, umbilical or valvular infections.

Typically large joints b/c of greater vascularization of the synovium.

Staph, Strep, Pseudomonas, etc. May also be fungal or rickettsial
Describe nonhematogenous infectious arthritis.
More common. Direct inoculation of joints - post-traumatic/post-sx, penetrating wounds, extension from adjacent tissues.
What are the synovial fluid alterations with septic arthritis?
Increase volume
Decreased viscosity
Increased cell numbers (predominantly neutrophils)
What is the pathophysiology of septic arthritis?
Synovial membrane inflammation leading to enzymatic degradation of articular cartilage.
What are the CS of septic arthritis?
Single limb lameness if non hematogenous.

Polyarticular if hematogenous.

Wt- to non-wt wearing lameness; swelling, pain, warm, may show systemic signs of pyrexia, anorexia and depression
Describe the trt of septic arthritis?
1) dx and mngmt of predisposing dz or disorder
2) ID of agent
3) Appropriate Abx at effective dosage
4) Drainage of Joint
5) Maintenance of jt motion (passive range of motion or continuous passive motion
6) Arthrodesis or amputation
What are the clinical signs of erosive arthritis?
Intermittent lameness & discomfort, increase in severity and frequency over time; bilat; systemic signs appear early; peripheral jts most often involved (carpus, tarsus, meta-carpus/tarsus)
What is the pathogensis of erosive arthritis (AKA Canine Rheumatoid arthritis/Idiopathic erosive PA)?
Altered endogenous antigen stimulates the production of host IgG and IgM AB (anti-IgG or rheumatoid factors), these AT-AB complexes form in the joint and activate complement --> leukotaxis and release of destruction enzymes pathologically alter the joint components

Dz perpetuated by T-lymphocytes
What tools/signs do you use to Dx erosive arthritis?
1) SF changes (increase volume, decreased viscosity, increased cell numbers)
2) SF biopsy - plasmacytic-lymphocytic infiltrate
3) Lab test - Rheumatoid factor, LE, ANA, etc
4) Rads
What are the pathologic lesions of erosive arthritis?
1) Villous hyperplasia of synovial membrane
2) Lymphoid and plasma cell infiltration of synovium
3) decreased viscosity of SF
4) erosion of articular cartilage and subchondral bone
Are NSAIDS useful in the trt of erosive arthritis?
No
What are some possible trts for erosive arthritis (Canine Rhuematoid arthritis)?
SADMOA, HA, Wt reduction, synovectomy or arthrodesis, euthanasia
Briefly describe Feline Chronic Progressive Polyarthritis.
Symmetrical non-infectious polyarthritis in two forms: periosteal proliferative form and erosive form.

Young-middle aged cats male

Etiolgoy may involve FeSFV, FeLV, synovium inflitrated w/ lymphocytes and plasma cells
What is nonerosive arthritis?
Synovitis from immune complex deposition, which can be immune mediated (Idiopathic) polyarthritis (most common), Chronic inflam-induced polyarthritis (Chronic dz, bacti infect, etc), Systemic Lupus Erythematosus (multisystemic dz assoc with renal, hemotologic, musclaur, cutaneous and nervous sys abnorm)
What are the therapeutic goals of treatment of osteoarthrosis?
Alleviate discomfort
Prevent further joint DJD
Restore joint function/mobility
Facillitate reparative processes w/in the joint
What two pathways can NSAIDs specifically (one pathway but not the other) or non-specifically (both pathways, or all the different parts of a single pathway) affect?
COX & LOX
What is the primary COX pathway you want to target?
COX-2 - Mediates pain and inflammation (inducible)
What is the COX pathway that when blocked causes the most side effects?
COX-1 because normally mediates platelet function, renal blood flow, and gastric mucosa protection (constitutive)
Why do you want to use NSAIDs?
To reduce proinflammatory mediators by inhibition COX 1&2 and LOX pathways.
What is a "wash-out" period?
The time you should allow in between switching from one NSAID to another - minimum 1-3 days, so you don't compound the side effects.
What is the medication you can administer along with NSAIDs to help protect against gastric lesions?
Misoprostyl (also Cimetidine and Omeprazole)
What Non-selective tradition NSAIDs should you never give?
Naproxen and Ibuprofen
What kind of asprin should you give and why?
Buffered asprin because protective effect on GI mucosa.
What effect does Asprin have on cartilage?
Asprin enhances cartilage degredation.
What are newer NSAIDs classified on?
COX inhibition
What two pathways can NSAIDs specifically (one pathway but not the other) or non-specifically (both pathways, or all the different parts of a single pathway) affect?
COX & LOX
What is the medication you can administer along with NSAIDs to help protect against gastric lesions?
Misoprostyl (also Cimetidine and Omeprazole)
What Non-selective tradition NSAIDs should you never give?
Naproxen and Ibuprofen
What Non-selective tradition NSAIDs should you never give?
Naproxen and Ibuprofen
What two pathways can NSAIDs specifically (one pathway but not the other) or non-specifically (both pathways, or all the different parts of a single pathway) affect?
COX & LOX
What is the primary COX pathway you want to target?
COX-2 - Mediates pain and inflammation (inducible)
What kind of asprin should you give and why?
Buffered asprin because protective effect on GI mucosa.
What is the COX pathway that when blocked causes the most side effects?
COX-1 because normally mediates platelet function, renal blood flow, and gastric mucosa protection (constitutive)
What effect does Asprin have on cartilage?
Asprin enhances cartilage degredation.
What is the COX pathway that when blocked causes the most side effects?
COX-1 because normally mediates platelet function, renal blood flow, and gastric mucosa protection (constitutive)
Why do you want to use NSAIDs?
To reduce proinflammatory mediators by inhibition COX 1&2 and LOX pathways.
What are newer NSAIDs classified on?
COX inhibition
What is a "wash-out" period?
The time you should allow in between switching from one NSAID to another - minimum 1-3 days, so you don't compound the side effects.
What are the 2 newer NSAIDs that target COX that can be used in cats?
Ketoprofen and Meloxicam
Is Ketoprofen nonselective or selective for COX inhibition?
Nonselective
What are 2 COX-2 preferential NSAIDs?
Carprofen and Meloxicam
Do the COX-2 preferential NSAIDs e.g. Carprofen and Meloxicam have significant side effects? What are they?
Yes, GI ulceration, vomiting, anorexia, possible liver and kidney dz.
What are the two drugs that are COX-2 specific?
Dercoxib and Firocoxib
What drug has more of a safety margin - Deracoxib (Deramax) or Firocoxib(Previcox)?
Firocoxib
What is the name of the drug that is a has both COX and LOX inhibition? For what species is it approved?
Tepoxalin (Zubrin), Dogs
What 3 things do chondroprotectives do?
1) Decrease enzymes that degrade cartilage matrix
2) Enhance chondrocyte metabolism
3) Increase synthesis of cartilage components
What does that administration of SADMOAs (Chondroprotectives) do when administered to patients with existing DJD?
1) Does not restore joint to normal
2) May protect against the development of further arthrosis
Provide an example of a slow acting disease modifying osteoarthritis agent.
Adequan canine
What is the MOA of SADMOAs?
Inhibit degenerative process and assist in healing process by stimulating chondrocytes to initiate cartilage repair.
Provide 2 examples of SADMOAs.
Cosequin and Glycoflex
How does Omega-3 FA use affect the dose of NSAIDs for OA?
Decrease the need for NSAIDs because antiinflammatory at the correct dosage.
What is the MOA for Omega-3s as a feed additive for dogs with OA?
1) Replacement of AA in cell walls with EPA decreases pain and inflam in arthritic joints
2) Blocks genes that cause inflammation in joints w/ OA
Wha is MSM and what properties does it have in relation to OA?
Methylsulfonylmethane (a derivative of DMSO) that has antiinflammatory and analgesic properties
What is HA and what is its MOA?
Hyaluronic Acid - non sulfated GAG which is the major component of proteoglycan aggregate in hyaline cartilage and SF.

MOA: increases viscosity of SF, antiinflamm, free-radical scavenger, boundary lubricant of synovial membrane
When would you use corticosteriods for DJD?
Advanced cases to improve QOL. Titrated to lowest effective dose using a short acting steriod. Seldom indicated and not amenable to more conservative trt because depresses chondrocyte metabolism and deleteriously alters proteoglycan and collagen synthesis.
What is osteochondrosis?
A disturbance of chondrocyte differentiation in the growth plate +/- articular cartilage, where the disturbance is in endochondral ossification.
What type of cartilage is in the growth plate and responsible for longitudinal bone growth?
Epiphyseal cartilage
When does endochondral ossification occur?
In growing animals. Normally the cartilagenous template will be replaced by bone.
What happens to the chondrocytes in OC? What about the pathology after this?
Chondrocytes multiply and become hypertrophic but fail to complete maturation --> focal areas of thickened cartilage that because of this thickening, nutrient diffusion is impaired and basal layers of the cartilage degenerate and undergo necrosis --> necrotic area is weaker and more vulnerable to trauma --> Fissures --> SF goes into fissures and contacts subchondral bone and causes inflamm --> cartilagenous flap!
What can happen to the OC cartilage flap?
1) May remain attached, preventing healing
2) May detach - resorbed or persist and form a joint mouse
What happens to untreated OCD?
Chronic joint inflammation and irreversible DJD.
What happens when osteochondrosis affects a growth plate?
Cartilage doesn't undergo necrosis (because of better vascularization in growth plate) - Thickened cartilage is structurally weak --> growth deformities.
What is the most clinically significant manifestation of OC of canine growth plate?
Cartilage core retention of the distal ulna
OC is multifactorial. What are some of these factors that influence the development of the disease?
- Excessive energy intake & rapid growth rate
- Hormonal influences
- trauma (early excessive exercise, inappropriate exercise surface)
-Hereditary/genetics
Where is should OC most apparent radiographically?
Mediolateral projection of the shoulder, flattening of the dorsocaudal humeral head, subchondral bone defect, sclerosis, etc.
What muscles typically atrophy with shoulder OC?
Infra and supraspinatus muscles
What conditions make up the Canine Elbow Dysplasia complex?
Humeral OCD, FCP, UAP and elbow incongruity.
How does a dog with the CED complex typically stand?
Elbows held close to chest wall.
What is elbow incongruity?
Humerus and radius and ulna do not fit well and the joint space is not parallel. Elliptical trochlear notch, shortened radius or ulna --> step length discrepancy.
What does the clinical signs of Stifle OC look similar to?
Hip dysplasia
What do you find on rads for stifle OC?
Flattening or defect in the medial aspect of the lateral femoral condyle, secondary osteoarthrosis prominent in early disease.
Where does the OC lesion typically occur in the hock?
Medial ridge of the talus (80%) - shown as flattening of the ridge, increased joint space and OC fragments
How do you trt asymptomatic OC? Prognosis?
Conservatively
Limited exercise, balanced diet, restricted energy intake, no mineral supplementation, chondroprotectives.

Asymptomatic lesion can heal with conservative mngmt.
What are the possible surgical trts for Osteochondrosis?
1) Arthrotomy/Arthroscopy
2) Remove offending cartilage flap
3) Stimulate subchondral bone to encourage and hasten cartilage repair (Curettage +/- drilling) --> defect will fill in with fibrocartilage
4) Reattach cartilage flap (OC of the talus - use K-wires)
5) Remove joint mice, FCP, UAP
6) Ulnar osteotomy
7) Augment Sx with anti-inflam drugs and chondroprotectives
Describe the prognosis for Shoulder, elbow, stifle and hock OC.
Shoulder: good-excellent. Best if trt early and no secondary DJD present

Elbow: fair to gaured. Depends on lesion, DJD will develop

Stifle: fair to gaurded. Defect can be very large. DJD will develop

Hock: gaurded to poor. DJD will develop
What is Canine Hip Dysplasia?
Most frequent hip dz
Hereditary, polygenic, multifactorial
Usually bilat, but can be unilat
Abnormal development of the hip leading to coxofemoral excessive laxity (subluxation) leading to osteoarthrosis
What are the most common breeds at risk for hip dysplasia?
Large and Giant breeds b/c of rapid growth rate.
T/F Cats don't develop hip dysplasia.
False
What are the CS/Hx for hip dysplasia before 6-8mo?
Abnormal gait (bunny hop, asymetric sitting position, waddling)
Usually no pain unless severe subluxation
What are the CS/Hx for hip dysplasia from 6/8mo to 10/12mo?
Uni/Bilat lamenes
Difficulty rising/jumping/climbing stairs, exercise intolerance
Waddling, stiff gait
Thigh amyotrophy
Pain

At this stage there is cartilage damage, release of inflammatory cytokines b/c of rubbing damage on femoral head.
What are the CS/Hx of hip dysplasia around 10-12mo?
+/- important functional improvement (b/c inflam becomes chronic)
Variable residual lamenes.
What are the CS/Hx of hip dysplasia at the long term?
Difficult rising, walking, jumping, running, climbing stairs; lameness worse in morning and after exercise, thigh amyotrophy, hip pain +/- crepitus

Chronic progressive signs due to the development of osteoarthrosis from damage to the cartilage.
What do you look for during an orthopedic exam as evidence of Hip Dysplasia?
Uni or Bilat hindlimb lameness
Thigh muscle atrophy
Pain during hip extension and abduction
Decreased range of hip motion
Instability (young dogs)
Crepitus (old dogs)
What are the DDx for Hip dysplasia?
- Trauma (fracture, luxation)
- Other osteoarticular pathologies of the young (eg. pannus)
- Infection: septic arthritis, osteomyelitis
- Neurologic problems
- Neoplasia: Bone, articular, nerve, ST
- Other: Immune mediated polyarthritis
How do you work up hip dysplasia?
Palpation
Radiographs
What do you do for palpation when trying to evaluate hip dysplasia?
- Dynamic Subluxation: Palpate greater trochanter of femur while they walk
- Passive subluxation --> Ortolani sign (angle of reduction to evaluate articular laxity) and Barlow sign (angle of subluxation to evaluate the acetabulum.
At what age can you do the OFA view? What are the advantages/disadvantages?
After 2 years.
Adv: Simple, well known, can evaluate laxity and osteoarthrosis
Dis or Inconvenients: evaluates unforced passive laxity. Need sedation, anesthesia
How does the OFA view evaluate joint laxity? (hip dysplasia)
Acetabular coverage (want more than 50% for a normal hip), articular zone, Norberg-Olsen angle
What does the OFA view consider to be evidence of OA/DJD for hip dysplasia?
Subchondral bone sclerosis, osteophytosis/enthesophytosis (morgan's line - osteophytes at capsular insertion)
Acetabulum/femoral head remodelling
T/F Radiographic signs of DJD for hip dysplasia are correlated to the intensity of the lameness
False
How old does a dog have to be for Penn Hip evaluation? What advantages does this provide? What about negatives?
>4weeks

- Evaluate passive forced laxity, early screening of predisposed dogs, prediction of development of OA
What is the DAR view?
Dorsal acetabular rim view - early screening for hip dysplasia
What test should be run on the follow categories of dog for hip dysplasia?
Pet (lame): Palpation, OFA
Pet (lame + future): Palpation, OFA, PennHIP, DAR
Breeding animal: Palpation, OFA, PennHIP, DAR
What are the treatment goals of Canine Hip Dysplasia?
- Prevention of degenerative changes
- Restoration of a functional articulation
- Improvement of patient comfort
What are the 3 components of medical treatment for hip dysplasia?
Weight control, adapted activity, medications
Why do you want to control weight in a hip dysplasia patient or a breed prone to hip dysplasia?
Overnutrition leads to rapid growth rates and excessive body weight increases the likelihood of phenotypic expression of CHD and OA.
What are the different components of physical therapy for canine hip dysplasia?
Passive Physical Therapy:
- passive ROM
- Heat/cold application
- Massages
- Electrostimulation
- Ultrasound, laser, shock wave
Describe heat and cold application during the first 2-3 days of medical treatment of hip dysplasia.
Cold application: vasoconstriction, decrease cell metabolism, edema, speed of sensorial conduction and spasms, analgesic

Heat after: vasodilation, muscle relaxation, increase some biochemical reactions, help tissue healing and analgesic.
What benefits to messages provide?
- Improve the vascular circulation
- Decrease muscle contracture and oedema
- Psycho-sedative effect.
With regard to exercise in the hip dysplasia patient, what is strictly forbidden? What benefits does adaptive physical activity provide?
Long term rest.

Improve muscle mass, provide dynamic joint stablization, improve cartilage nutrition and lubrication, help preserve range of motion.
What antiinflammatory drugs can you consider for treatment of canine hip dysplasia?
NSAIDs
- Non/little specific: ketoprofen, tolfenamic
- COX 2 preferential: carprofen, meloxicam
- COXIB (COX2 Specific): Deracoxib, firocoxib
- COX/LOX: tepoxalin

Others: tramadol, gabapentin

Corticosteriods (not good long term)
What are the types of preventative surgical treatments for canine hip dysplasia?
Juvenile pelvic symphysiodesis

Triple Pelvic Osteotomy
What are the types of curative or palliative surgical treatment for canine hip dysplasia?
Total Hip Replacement
Hip Capsular denervation
Femoral head and neck ostectomy
What are the principles, candidates, advantages and disadvantages for Juvenile pelvic symphysiodesis?
Principle: increase head coverage by stopping pubis growth

Candidates: dogs <5mo

Adv: low cost, easy, low morbidity

Disadv: early detection
What are the principles, candidates, advantages and disadvantages for Triple Pelvic Osteotomy?
Principle: increase femoral head coverage by rotating the acetabulum. Involves fracturing and realigning the ilium, ischium & pubis.

Candidates: No OA (important)

Adv: Propylactic

Disadv: cost, specialist, complications, post-op

>90% success rate
What are the principles, candidates, advantages and disadvantages for total hip replacement?
Principle: replace OA hip by a prosthetic one

Candidates: all dogs (can have DJD etc)

Adv: excellent outcome

Disadv: cost, specialist, complications
What are the principles, candidates, advantages and disadvantages for hip capsule denervation?
Principle lower pain by cutting senstive nerves

Candidates: all dogs w/ OA

Adv: easy, low cost, low morbidity/complications

Disadvantage: palliative (will not be normal but decreased pain)
What are the principles, candidates, advantages and disadvantages for femoral head & neck ostectomy?
Principle: Removal of the femoral head and neck - "no articulations, no pain." Basically turns the hind limb into a forelimb.

Candidates: every dog

Advantage: easy, low cost, low morbidity/complications

Disadvantage: palliative, salvage procedure

Results are good but variable
What is the most common luxation in small animals?
Coxofemoral luxation (Hip luxation)
What is the most common form of coxofemoral luxation? What usually causes it?
Craniodorsal displacement of the femoral head from the acetabulum.

Secondary to trauma (vehicular trauma and falling)
What is the pathophysiology of coxofemoral luxation?
joint capsule is usually torn as is the round ligament of the femoral head. Hemorrhage fills the acetabulum & fragments of capsule and ligament. Gradually organizes into a fibrous mass which can interfere with manual reduction after a few days.

With chronic luxation articular cartilage degeneration occurs.

Portions of the acetabular rim can be fractured or a portion of the femoral head may be avulsed.

Immature dogs usually sustain capital physeal fracture rather than luxation.
How does a dog with craniodorsal coxofemoral luxation usually hold their leg?
Thigh adducted and stifle externally rotated, affected lim appears shorter, great trochanter is elevated. Distance b/w the greater trochanter and tuber ischii is INCREASED and alteration of coxofemoral triangle.
What is the coxofemoral triangle?
Crest of ilium, ischiatic tuberosity and greater trochanter. With hip dislocation the line is nearly straight.
What are your trt options for CLOSED reduction w/ coxofemoral luxation?
Manipulative technique
DeVita pinning (provides additional support to hip to lessen likelihood of reluxation.
What are the indications for open reduction of coxofemoral luxation?
1) chronic, recurrent or unstable luxations after closed reduction
2) Luxations w/ avulsion fx of femoral head or acetabulum
3) Polytramatized patient
What are the different techniques for open reduction of coxofemoral luxation?
Capsulorrhaphy
Placement of a prostetic joint capsule
Transposition/relocation of the greater trocanter
Transarticular pinning
Femoral head and neck excision and total hip replacement (salvage options)
When is it indicated to use a prosthetic joint capsule for coxofemoral luxation?
Insufficient jt capsule reamins
If the jt capsule has been stripped from dorsal acetabular rim or femoral neck
What is aseptic necrosis of the femoral head?
Progressive necrosis of the femoral head with the resultant collapse and distortion of the femoral head.

Legg-Perthes Dz
T/F With aseptic necrosis of the femoral head there is usually histological evidence of infarction or epiphyseal and metaphyseal bone.
True
What are some of the clinical signs of aseptic necrosis of the femoral head?
Unilteral weight-bearing lameness of the hindleg - slowly progressive, may carry limb at faster gaits. Crepitation, muscle atrophy.
What are some of the treatment options for aseptic necrosis of the femoral head?
Conservative trt: Ehmer sling, strict rest for one month (for the small % that revascularize and femoral head won't collapse)
Sx trt: femoral head and neck excision, intensive physio.
What is the most common cause of lameness in the dog?
Disorders of the stifle
What should you do when examining a dog for stifle lameness?
Observe the dog walking
Assume position caudal to the standing dog and assess symmetry, effusion, fibrous proliferation of the medial aspect of the joint.

Then position in lateral recumbency - full range of motion, crepitation and meniscal click, internal and external rotation of the stifle, varus or valgus, position of the patella.

Cranial and caudal drawer tests

Tibial compression test
A cranial drawer of ___ is suggestive of CCL rupture?
>2mm
T/F. A positive cranial drawer test in flexion but not extension suggests an isolated rupture of the craniomedial band of the CCL (caudolateral band remans in tact). This is a partial tear.
True
T/F The tibial compression test for cranial tibial thrust is more sensitive than cranial drawer because it occurs before evidence of cranial drawer.
True
Where is the normal point of contact of the tibia and femur on the lateral view?
Middle third of the condylar arc. A more caudal point of contact suggests CCL rupture. A more cranial point of contact suggests CaCL rupture.
T/F Osteophytes can be seen with CCL rupture?
True (usually w/w 2 weeks of the insult)
T/F Severity of DJD is directly propotional to the dogs size.
True
Why does instability decrease with chronicity with respect to CCL rupture?
Periarticular fibrosis
___ is the most common cause for lameness in the dog and most common cause for osteoarthrosis of the stifle in dogs.
CCL rupture
What are the causes of CCL rupture?
Traumatic (forced hyperextension or rapid internal rotation)

Degenerative (ligament deteriorates in older dogs)
Describe the rapid secondary joint changes seen with rupture of the cranial cruciate ligament. STIFLE - NOT ON MIDTERM
Hyperplasia of the medial soft tissues and the collateral ligament, osteoarthrosis (more rapid in large dogs), meniscal injury.
T/F Conservative mngmt is adequate for most dogs less than 10kg for rupture of the cranial cruciate ligament.
True.
T/F surgical trt is the trt of choice for most large dogs and carries a better prognosis. (85-90% success rate)
True
What are the possible surgical techniques for ruptured CCL?
Arthrotomy (remove remnants of CCL, evaluate DJD and remove osteophytes, inspect menisci)

Intra or extracapsular
Why is primary repair of the CCL not possible?
Small size of the ligment, degenerative changes and poor blood supply.
What is scapular luxation?
Rupture of scapula supporting muscles - serratus ventralis, rhomboideus & trapezius, resulting in dorsal displacement of scapula and forelimb.
How do you treat scapular luxation?
Medical: closed reduction + Velpeau bandage.

Surgery: repair of torn muscles (usually not possible) + reinforcement (caudal scapula sutured/wired to adjacent 5, 6 or 7th rid).
T/F Lateral shoulder luxation is more common than medial.
False. Medial is more common.
What are the medial shoulder luxation characteristics?
Congenital, small & miniature breeds predisposed, dogs are often affected bilaterally, chronic forelimb lameness, young age, w/o history of trauma
With medial shoulder luxation, how is the limb held?
May not be very lame or painful, limb held in flexion, abduction, and external rotation. Acromion very prominent on palpation, difficulty extending the shoulder, shoulder luxates medially easily.
What is the conservative management for medial shoulder luxation?
Exercise restriction and analgesia. Can attempt closed reduction if good congruency & minimal DJD
What are the characteristics of lateral shoulder luxation?
TRAUMATIC in origin, primarily LARGE BREEDS, any age, acute onset non-weightbearing forelimb lameness. LESS COMMON than medial!
What do you usually see on an orthopedic exam with lateral shoulder luxation?
Limb held in flexion, adduction and internal rotation. Acromion difficult to find, greater tubercule prominent
Should you always try conservative management with lateral shoulder luxation?
Yes.
Why do you want to have the limb held in extension before attempting closed reduction in certain procedures eg. lateral should luxation reduction.
Better muscle relaxation therefore easier to do reduction.
What are your surgical options of open reduction and stabilization of shoulder luxation?
Imbrication of the joint capsule, prosethic suture stabilization, tendon transposition (biceps brachii or supraspinatus)
What is shoulder instability?
"Emerging dz" probably more frequent than expected, pathologic increase in ROM of joint due to tearing, streching of supportive structures resulting in subluxation
What are your best diagnostic techniques for shoulder instability?
U/S, MRI (best). SA Sx Textbooks say Arthroscopy is used for definitive Dx???
What can you do to treat shoulder instability?
Medical mngmt - rest & rehabilitation

Surgical mngmt - open or arthroscopy.
What is biceps tendon disease?
Bicipital tenosynovitis: inflammation of tendon of the biceps brachii and surrounding synovial sheath.

Tear (partial or complete) of biceps brachii tendon.

Middle age, medium to large breed active dogs or older out of shape dogs.

Chronic intermittent or progressive lamness worse after exercise or acute onset after blunt trauma.
What tools can you used to dx biceps tendon disease?
Radiography
Positive contract arthrography
U/S
Arthrocentesis & SF cytology
Arthroscopy (definitive dx according to SA Surgery Textbook) and MRI
T/F Conservative mngmt should be attempted before surgery in biceps tendon dz.
True
Biceps tendon dz should be treated with surgery when medical trt yields unsatisfactory outcome. What methods can you use?
Tenodesis: transection of the tendon and transposition of the origin to the proximal humerus...or transposition of the bicipital tendon laterally out of the intertubercular groove.

Biceps brachii tenotomy
What are the characteristics of traumatic elbow luxation?
90% lateral, traumatic in origin, any breed, any age, acute onset on non-wt bearing forelimb lameness.
What do you see on an orthopedic exam with traumatic elbow luxation?
Limb carried in flexion, abduction and external rotation, joint swelling and pain, elbow will not flex or extend
T/F Conservative management should always be attempted ASAP in acute cases of traumatic elbow luxation with no fractures.
True
Explain the 3 different types of sprain related to carpus/tarsus ligament injury.
Sprain 1st degree: inflam, hematoma (stretched ligament)

Sprain 2nd degree: partial rupture (some instability but ligament remains)

Sprain 3rd degree: Complete rupture, v. severe trauma
What are the 3 groups of carpus tarsus instability and sublux/lux? i.e. what are the types of rupture
- Collateral ligament rupture
- Palmar ligament rupture
- Other ligament rupture
What are the important carpal ligaments?

What are the important tarsal ligaments?
Carpal: Med & lat collateral, palmar carpal fibrocartilage

Tarsal: Med & lat collateral, tarsal fibrocartilage
If you have an injury to the MCL what kind of instability do you see?
See excessive medial opening of the joint space leading to VALGUS (feet go laterally)
If you have an injury to the LCL, what kind of instability do you see?
See excessive lateral opening of the joint space leading to VARUS (feet go medially)
If you have a carpal/tarsal hyperextension injury, what do you see?
Plantigrade/palmigrade stance causing instability, excessive plantar/palmar opening
What is the purpose of plain radiographs and stress rads in carpal/tarsal instability/lux?
Plain - to r/o other dz

Stress - ID lesion and localize it
What is the best option for trt of complete rupture of the collateral ligaments of the distal limb?
Conservative mngmt is NOT the best!

Sx - protect/replace w/ prosthetic ligament screws/suture spanning the involved articulation so that it is more stable while scar tissue is building. Try to mimic the origin and insertion of the normal ligament.
What is the best option for treatment of hyperextension injury of carpus/tarsus?
Arthrodesis - depending on level of instability (partial or complete)

Splinting is never successful!
What is the prognosis for collateral ligament rupture or hyperextension injury with appropriate trt?
Excellent!
What is the main area of fracture of the distal forelimb?
Styloid process
What is generally the best trt option for distal limb fractures?
Surgery
What is a shearing injury? How should it be trted?
An severe injury to a distal limb primarily due to HBC with ST, bone and articulation involvement. Emergency trt is to tend to the wound - shave, clean, explore, debride, bandage, second intention healing. Want to provide stability, repair the fx and preform salvage procedure if necessary.
What is laxity syndrome in the distal limb?
"Carpal flexural deformity" - hyperextension or hyperflexion of carpal joint of unknown etiology of young puppies and is self-limiting. Trt with adequate exercise on solid footing, DON'T splint or cast.
In what species do you typically see a sesamoid fx of the metacarpus/tarsus/phalanges?

What about metacarpal or phalanx fx?
Sesamoid fx: greyhound, rottie
Meta/Phalanx: stress fx of greyhound
How do you decide how to treat a metacarpal/tarsal fx? i.e. when do you decide to use external coaptation or surgery?
External coaptaiton if incomplete fx, minimal displacement or only involved 1 or 2 bones

Sx if involves more than 2 bones (MC III or IV), segmental or comminuted fx
How are most fractures of the phalanges treated?
External coaptation.
When should you attempt conservation management with a sesamoid fracture?
Attempt 1st (cast and activity restriction)
What is an arthrodesis? When is an arthrodesis indicated?
Surgical bony fusion across a joint space when there is no remaining option (i.e. it is a salvage procedure).

Arthrodesis is indicated when there is chronic joint instability, irreparable fx involving a joint, severe/chronic DJD or neurologic deficits.