Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Large Animal Surgery > Equine Joint Disease > Flashcards

Equine Joint Disease Flashcards

1
Q

What is osteochondrosis?

A

failure or endochondral ossification, which leads to ischemic necrosis of the epiphyseal cartilage due to interruption of cartilage canal blood supply

= chondronecrosis with necrotic, non-perfused cartilage canals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is osteochondrosis manifesta?

A

progression of OC, which impedes mineralization or vascularization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are 3 possible results from osteochondrosis manifesta?

A
  1. lesion surrounded by bone is replaced by fibrous tissue and undergoes membranous ossification
  2. sunbchondral cyst - weight bearing results in unfolding of cartilage (secondary to trauma)
  3. osteochondrosis dissecans (OCD) - rupture of overlying cartilage results in fissure formation (secondary to trauma)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are 6 possible etiologies of OC?

A
  1. biochemical influences
  2. failure of vascularization
  3. nutrition - mineral (Ca, P) imbalances, CHO (aldehyde) levels
  4. hormonal factors
  5. growth rate
  6. genetics

multifactorial!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What 4 breeds are associated with developing OC? What signalment is associated?

A
  1. TB
  2. WB
  3. QH
  4. Draft horses

yearlings or at he start of training (2-3 y/o)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is clinical sign is indicative of OC?

A

joint effusion - “boggy hocks” (bog spavin) –> NOT lame at this time, possible with larger fragments

  • bilateral is COMMON
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the most important diagnostic tool for OC?

A

radiographs

  • lameness exam can be abbreviated based on clinical signs and signalment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What 4 joints are affected by OC in order of occurrence?

A
  1. tibiotarsal joint (hock) - distal internal ridge of the tibia (DIRT), lateral > medial
  2. femoropatellar joint (stifle) - lateral femoral trochlear ridge > medial
  3. metacarpophalangeal/metatarsophalagneal joints - dorsal sagittal ridge > dorsal P1 > plantar P1
  4. scapulohumeral joint - glenoid, humeral head

more distal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the 5 structures most commonly develop subchondral bone cysts as a result to OC?

A
  1. medial femoral condyle, phalanges**
  2. carpal bones, tibia
  3. distal radius, talus
  4. sesamoid bones (including NB)
  5. humerus

(may or may not affect joint)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How is OCD treated?

A

arthroscopic removal

  • can only be managed conservatively with no effusion or lameness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the most common procedure done to treat subchondral bone cysts? What are 4 other options? What is not recommended?

A

surgical cyst debridement + intralesional corticosteroids (can be ultrasound-guided to avoid sx)

  1. bone scaffold implantation
  2. cartilage flap transplant
  3. regenerative therapies
  4. transcondylar screw

medical management - rarely effective (~30%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

In what timeframe of development/change is expected for OC? What does this mean for clients?

A
  • STIFLE - can change for up to 9 months
  • HOCK - can change for up to 6 months
  • NOT a static lesion

> 1 year without signs is considered “safe”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is osteoarthritis? What are 3 parts of its pathogenesis?

A

equine degenerative joint disease (DJD) affecting the articular cartilage and subchondral bone

  1. abnormal mechanical loads - abnormal load on normal cartilage or normal load on abnormal cartilage
  2. metabolic tissue failure due to catabolic processes overwhelming anabolic repair
  3. this leads to cartilage having little to no ability to repair itself since it depends on diffusion of synovial fluid for nutrients
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the 2 most common causes of abnormal loads on cartilage of horses that lead to OA?

A
  1. athletic use
  2. poor conformation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Why is the quality of tissue repair slow and imperfect? What is the most common result of healing? What does this depend on?

A

cartilage is avascular and lacks growth factor stimulation - full thickness lesions do not heal and partial thickness lesions have negligible healing

poor adhesion with fibrocartilage

age, species, size, location –> young > old, weight-bearing > non-weight-bearing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What healing occurs when cartilage is gone?

A

fusion

  • osteophyte and enthesophyte formation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the single greatest economic loss in the equine industry?

A

articular disorders

  • joint replacement is not possible in horses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are 4 signs of OA?

A
  1. loss of RoM and lameness
  2. joint effusion
  3. heard swelling around joint - advanced disease, periarticular new bone formation
  4. axial muscle soreness - back pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are 3 options for diagnosing OA?

A
  1. lameness exam - positive flexion, blocks
  2. radiographs +/- MRI, CT
  3. response to treatment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are 6 radiographic features of OA?

A
  1. periarticular osteophytosis
  2. asymmetrical joint space thinning
  3. subchondral sclerosis
  4. subchondral lysis
  5. osteochondral bodies - disintegration of joint surfaces, fractured osteophytes
  6. advanced remodeling or ankylosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the 4 goals when treating OA?

A
  1. decrease inflammation
  2. prevent further cartilage damage - fixing is not possible
  3. alleviate pain
  4. return to function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are 6 systemic treatments for OA?

A
  1. NSAIDs
  2. hyaluronic acid
  3. polysulfated glycosaminoglycans
  4. pentosan (?)
  5. nutraceuticals
  6. osteoclast inhibitors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are 7 local treatments for OA?

A

MEDICATIONS - corticosteroids, HA, polyacrylamide hydrogel (PSGAGs)

BIOLOGICS - IRAP, PRP, Pro-stride (IRAP + PRP), stem cell therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is hyaluronic acid? What effect does it have? What is the typical treatment protocol?

A

component of synovial fluid and cartilage ECM

anti-inflammatory

Legend ($84/vial) - 40 mg IV (1 vial) weekly for 1-3 treatments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Where do systemic PSAGAGs come from? What are 2 possible mechanisms?

A

chondroitin sulfate from bovine lung and trachea

  1. inhibits inflammatory cytokines
  2. upregulation of GAGs and collagen synthesis
26
Q

What is the typical treatment protocol with systemic PSGAGs? What must also be added? What may be some other options?

A

Adequan ($32/dose) - 500 mg q 4 days for 7 treatments IM or 250 mg up to once a week for 3-5 weeks

antibiotic - increased risk of septic joint

limited evidence for $$$ treatment - compounding, Pentosan

27
Q

What are the 2 building blocks of cartilage that should be included in oral nutraceuticals?

A
  1. chrondroitin sulfate
  2. glucosamine

NOT FDA approved, recommend “name” brands like Cosequine and Platinum

28
Q

What are 2 options for systemic osteoclast inhibitors? What are 4 side effects?

A
  • Tiludronate (Tildren) - IV 1 mg/kg in 1 L bag over 90 min –> $195 for 30 mL
  • Clodronate (Osphos) - IM 13 mL for 1000 lb horse in 3 sites, may take 50 days for effect –> $215 for 15 mL
  1. transient colic
  2. may affect bone growth/healing (not studied in <4 y/o)
  3. nephrotoxic if given with NSAIDs
  4. long-term effects not studied
29
Q

What are 2 pros and 3 cons to using corticosteroids in treating OA?

A

powerful and long-acting + cost-effective

  1. inhibition of chondrocyte metabolism at high doses (chondroprotective and anti-inflammatory at LOW doses)
  2. laminitis
  3. septic arthritis or non-septic synovitis (joint flare)
30
Q

What corticosteroids are recommended for high and low motion joints?

A

HIGH MOTION - triamcinolone (medium duration, 5x potency compared to hydrocortisone), betamethasone (med-long duration, 30x potency compared to hydrocortisone)

LOW MOTION - methylprednisolone (med-long duration, 5x potency compared to hydrocortisone)

31
Q

What are 4 disadvantages to using corticosteroids for treating OA?

A
  1. steroid arthropathy - low incidence, narrowed joint space, joint instability, osteonecrosis
  2. immunosuppressive - MUST use aseptically, aseptic arthritis
  3. post-infection flare - self-limiting, can use NSAIDs, DDx septic arthritis
  4. laminitis
32
Q

What kind of hyaluronic acids work best for treating OA? What protocol is recommended?

A

higher molecular weight (>500 kDa)

intra-articular 20 mg/joint once a week for 3 weeks (Hyvisc = $65/dose)

33
Q

What do hyaluronic acids work synergistically with?

A

triamcinolone - often given with corticosteroids

34
Q

What are IRAPs? How do they work?

A

interleukin-1 receptor antagonist protein (autologous conditioned serum)

uses horse’s own serum to reproduce IL-1, leading to potent anti-inflammatory effects by blocking proinflammatory IL-1

(takes <24 hr to prepare, $1000-1500)

35
Q

Where is platelet-rich plasma most commonly used? How does it compare to IRAP?

A

tendons > joints

more convenient with stall-side kits + cheaper ($800/tx)

36
Q

What is Pro-Stride?

A

stall side autologous protein solution device that uses both IRAP and PRP

37
Q

How are mesenchymal stem cells (MSCs) used to treat OA? What are 3 possible sources? How long do they take to prepare?

A

cells are placed at the site of pathology, where they will differentiate themselves into the tissue needed to heal and replace the pathologic tissue with normal tissue

BM, embryonic, adipose

3-4 weeks (10-25 million cells/tx) –> $2500-4000

38
Q

What 3 management considerations should be taken for patients with OA?

A
  1. exercise - worse on stall rest!
  2. shoeing/trimming - biomechanical advantage
  3. diet - obesity is not helpful
39
Q

When is surgical treatment for OA used? What are 2 options?

A

when medical treatment is not working

  1. arthrodesis - implants ($3-5K)
  2. facilitated ankylosis - substance or procedure to promote fusion (drilling, ethyl alcohol, LASER)
40
Q

OA treatment guide:

A
41
Q

What are the most common etiologies of septic arthritis?

A
  • traumatic***
  • iatrogenic**
  • hematogenous*
  • peri-articular infection spread
  • idiopathic
42
Q

What 3 bacteria most commonly cause septic arthritis? Why is diagnosis often delayed?

A
  1. Enterobacteriaceae
  2. Staph
  3. Strep
  • horse owners don’t know anatomy
  • doesn’t seem bad initially
  • lameness is typically delayed
43
Q

What are 4 risk factors for developing septic arthritis?

A
  1. medication - PSGAGs (250 mg), corticosteroids mask signs for up to 3 days –> S. aureus
  2. clipping
  3. large gauge needle (>20 g)
  4. reusing needles –> ONE poke only
44
Q

In what horses is hematogenous spread the most common cause of septic arthritis? What is the pathogenesis?

A

foals <30 days of age (50% >1 joints affected)

  • partial or complete failure of passive transfer
  • immunocompromised
  • bacteremia
  • bacterial settle in joints due to low blood flow and low O2 tension in tissues
45
Q

What is the most common cause of hematogenous septic arthritis? What are 3 examples?

A

Gram-negative (Enterobacteriaceae)

  1. E. coli
  2. Salmonella
  3. Pseudomonas
    (+/- Enterobacter, Acinetobacter, Proteus, Klebsiella, Citrobacter)
46
Q

What causes hematogenous septic arthritis in adults?

A

RARE - Gram +

47
Q

How is septic arthritis diagnosed?

A
  • arthrocentesis +/- pressurization - cytology, C&S
  • radiographs
  • contrast radiograph or fistulogram
  • ultrasonography
48
Q

What is done with samples taken from arthrocentesis? What are 6 characteristics of normal synovial fluid?

A

collect in purple top for cytology and red top for culture

  1. pale yellow and clear
  2. does not clot
  3. TP <2 g/dL
  4. WBC cell count <500 cells/uL
  5. viscous
  6. strings 5-7 cm out of syringe or 1-1.5 cm between fingers
49
Q

What fluid is used for fluid pressurization? What different volumes are used for 6 joints?

A

sterile saline

  1. tibiotarsal - >40 mL
  2. radiocarpal - >15 mL
  3. intercarpal - >15 mL
  4. metacarpophalangeal - >13 mL
  5. MFT & LFT - ~60 mL per pouch
  6. PF - ~120 mL
50
Q

What is the purpose of using radiographs for septic arthritis? What is important to note?

A

determine bone involvement, which decreases prognosis - osteomyelitis and physitis common in foals

changes can take weeks to months to develop

51
Q

What is the purpose of performing contrast radiographs?

A
  • determine wound communication
  • see cartilage defects
52
Q

What are 5 uses of ultrasonography for septic arthritis? What joints is it best used for?

A
  1. communication with wound (air artifact)
  2. evaluate effusion and nature of fluid
  3. evaluate some areas of particular cartilage
  4. identify FB
  5. assess synovial inflammation

those hard to palpate or image

53
Q

What is the ideal solution for treating septic arthritis? What is considered gold standard? What is another option?

A

refer, especially as iatrogenic

arthroscopic lavage - bigger portals able ot remove fibrin and other debris ($2K)

through and through lavage - not appropriate for cases with fibrin accumulation, large needles

54
Q

When are local antimicrobials indicated for septic arthritis? What are 3 advantages and 1 disadvantage?

A

any local infection based on C&S

  1. high concentrations able to be used
  2. decreased systemic toxicity
  3. cost effective

harmful vascular or cartilage sequela

55
Q

What are 5 options for delivery methods for local antimicrobials?

A
  1. regional IV perfusion
  2. regional IO perfusion
  3. intrathecal
  4. PMMA or POP impregnated with antibiotics
  5. other products containing antibiotics
56
Q

What is the most likely organism that causes septic arthritis? What is the most common type of antibiotics used? What else can be used?

A

Staph - still use C&S to identify isolate of the area

water-soluble, concentration-dependent - Aminoglycosides (SID or EOD)

time-dependent - tissues serve as antimicrobial depot after tourniquet is released (will likely need more than once a day, increases chance of phlebitis)

57
Q

When are systemic antibiotics indicated for treating septic arthritis? What is used?

A

infection is suspected

broad-spectrum until C&S results –> Amikacin + Cephalosporin, Penicillin + Gentamycin

(ineffective on their own, maximal concentration lags behind plasma levels)

58
Q

What are 6 ancillary treatments used for septic arthritis?

A
  1. pain management
  2. hyperbaric oxygen therapy
  3. surgery - annular ligament release
  4. wound care
  5. laser therapy
  6. rest and PT
59
Q

What is prognosis of septic arthritis in adults like?

A
  • 54-85% survive
  • 33-77% return to work
60
Q

In what 4 situations are foals with septic arthritis less likely to be able to race?

A
  1. multisystemic disease
  2. Salmonella isolated
  3. multiple joints
  4. > 95% neutrophils in synovial fluid

(if returned, takes longer until started in first race)

Large Animal Surgery (32 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions