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3. Cat & Dog 2 > Management of OA > Flashcards

Management of OA Flashcards

1
Q

Osteoarthrosis other names

A

“OA”, osteoarthrosis, Degenerative Joint Disease, DJD,
* (Arthritis, Osteoarthritis)

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2
Q

OA definition

A

Non-inflammatory degenerative joint disease leading to Progressive, IRREVERSIBLE, degeneration of articular cartilage

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3
Q

OA can leaad to what type of inflammation

A
  • Low-grade non-suppurative inflammation
    <><>
  • But remember that OA is a non-inflammatory process overall
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4
Q

what anatomic structures does OA affect?

A

Affects the ENTIRE joint +other systems
* Cartilage degradation
* Osteophyte formation
* Subchondral bone remodeling
* Periarticular tissue changes (i.e., fibrosis)
* Neural sensitization…

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5
Q

primary OA etiology, prevalence, risk factors…

A

PRIMARY
* Infrequent: Prevalence unknown
* Genetic predisposition, age , obesity…

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6
Q

secondary OA prevalence, etiology, cause, anatomic locations

A

SECONDARY
* MOST COMMON IN SMALL ANIMALS
* Caused by another disease affecting the joint
* Fracture, elbow dysplasia, hip dysplasia etc…
ALWAYS LOOK FOR THE CAUSE!

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7
Q

secondary OA pathogenesis

A
  1. Normal stresses + abnormal joints
    OR
  2. Abnormal stresses + normal joints
    => Production of inflammatory mediators and enzymes by chondrocytes and synoviocytes (I)
    > prostaglandins
    > collagenases
    > proteinases
    > interleukin
    > etc…
    => all leads to cartilage degradation, which causes more inflammatory mediators… etc…. in a feedback loop
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8
Q

OA morphologic changes

A
  • low grade synovitis
  • Cartilage loss and subchondral bone sclerosis
  • Marginal Osteophytes
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9
Q

OA joint flulid changes

A
  • Inflammation increases the protein content of synovial fluid and changes permeability of synovial barrier
    <><><><>
    Degradation of proteoglycans
  • Decreases viscosity and quality
  • Alters oncotic/osmotic balance
    > ** Joint Effusion**
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10
Q

OA diagnosis - history

A
  • Slowly progressive, initially low grade lameness
  • Intermittent to permanent
  • Worse after period of rest or over-exercise
  • Respond well to NSAIDS
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11
Q

OA diagnosis - physical exam

A
  • Joint pain / lameness (mild–moderate)
  • Effusion
  • Joint capsule thickening
  • Crepitus
  • Decreased range of motion
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12
Q

purpose of ancilliary tests for OA?
what tests can we do? what are their characteristics?

A
  • Rule out other disease processes
  • Identify cause
  • Assess overall health of patient
    <><><>
  • Radiographs: Poorly sensitive but SPECIFIC
    > Effusion, osteophytosis (>2 weeks), sclerosis
  • CT: More sensitive than radiographs
  • Arthrocentesis
  • Arthroscopy: Direct visualization
  • (Blood work)
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13
Q

arthrocentesis results for OA
- volume
- viscosity
- appearance
- cell count
- cell type

A
  • volume: inc. + to ++
  • viscosity: decreased > normal is viscous, inflamed or septic is watery
  • appearance: clear-turbid > normal is clear, inflamed or septic is more turbid
  • cell count: <5000/mcl > normal is <3000, inflamed or septic is more marked increase
  • cell type: Mono, PMN <12% > normal is Mono, PMN <12%, inflamed or septic is just PMN >12%
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14
Q

Management of Osteoarthrosis
- aims? what can we do?
- specific plans?

A
  • No cure
  • Alleviate pain and discomfort
  • Reduce and control inflammation
  • Minimize further cartilage degeneration
  • Improves joint mobility
  • Increase activity level
  • IMPROVE QUALITY OF LIFE
    <><><><>
  • Identify and correct primary cause
  • Clinical signs are highly variable
    <><><><>
  • Weight Management!
  • 5 to 8% weight loss significantly improve
    lameness scores
    <><><><>
    Lifestyle modification and physical rehabilitation
  • Rest if flare-up
  • Moderate but regular exercises
  • Avoid intense activity
  • Avoid unnecessary concussive activity
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15
Q

how much weight should we lose to improve lameness scores with OA?

A

5 to 8% weight loss significantly improve
lameness scores

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16
Q

Lifestyle modification and physical rehabilitation strategies for OA

A
  • Rest if flare-up
  • Moderate but regular exercises
  • Avoid intense activity
  • Avoid unnecessary concussive activity
17
Q

rehabilitation for OA - does it have benefits? like what?

A

Benefits mostly extrapolated from human but evidence is growing…
* Treating pain
* Maintain joint mobility
* Maintain muscle mass
* Improves well-being
*…

18
Q

Management of Osteoarthrosis - what drugs do we give? what is our first choice? how much do we give?

A

Anti-inflammatory drugs
* NSAIDs (generally first choice)
> As required with rest (during flare-ups, after/before activity…)
> Lowest dose effective
> Safety!…they are generally safe but not benign…
=> Blood work, exam, UA, beware of “off label” use …

19
Q

Management of Osteoarthrosis: NSAIDS
- which should we use?

A

No clear winner…if one does not work, try another
* Meloxicam (No limit in dog, Max 5 days cats…)
* Robenacoxib (No limit in dog, Max 6 days cats…)
* Deracoxib (Not cats)
* Carprofen (Not cats)
* Gapriprant – Prostaglandin receptor antagonist (Not cats)

20
Q

non-NSAID drugs we can use for management of OA?

A
  • Amantadine > NMDA receptor agonist, used to treat neurogenic pain… 1 study in dogs
  • Gabapentin > GABA agonist used to treat neurogenic pain… no studies in dogs or cats
  • Amitryptiline > antidepressant
  • Tramadol synthetic Mu agonist
    > Most recent study show no efficacy compared to placebo in dogs
    <><><><>
  • Intra-articular Corticosteroids
    > Limit their use, strict rest.
    > Generally when other therapies have failed
21
Q

Disease Modifying Agents (DMOAs) that have been used for OA?
how do we administer? use / efficacy?

A
  • Polysulfated glycosaminoglycans (Adequan) (bovine tracheal cartilage)
  • Pentosan Polysulfate (Cartrophen) (from hemicellulose, structure similar to heparin)
    <><><>
  • Injectable
  • Mechanism of action unknown
  • Moderate level of comfort recommending usage
  • Efficacy? (anecdotal)
22
Q

Nutritional Management for OA - how useful?

A

Glucosamine sulfate
* Influence on chondrocyte metabolism?
* Not enough evidence to support use?
<><><><>
Chondroitin sulfate
* Anti-inflammatory effect?
* Not enough evidence to support use?
<><><><>
* Omega 3 fatty acids

23
Q

omega 3 fatty acids - use for OA? mechinism?

A
  • Probably the highest level of comfort
  • “Hijacks” the inflammatory cascade by replacing omega 6FA
    <><><><>
    Joint diets:
  • Hill’s J/D
  • Royal Canin Mobility
  • Purina JM
24
Q

Mesenchymal stem cell therapy for OA
- what is the goal? does it work?

A
  • Regenerative therapy?
  • Mostly stromal cells, few stem cells…
  • Immunomodulation through paracrine effect or
    soluble factors released in the solution?
  • Evidence not strong!
25
Q

Platelet Rich Plasma (PRP) for OA - does it work?

A
  • Large variability in preparation technique
  • Same mechanism of action as stromal cells?
  • Not enough evidence
26
Q

Hyaluronic Acid (HA) for OA - goal? efficacy?

A
  • Restore viscosity of synovial fluid
  • Evidence not strong
27
Q

OA Take Home Message
- mostly primary or secondary in dogs and cats?
- what does it lead to?
- Dx?
- Tx goals and strategies?

A
  • OA is generally SECONDARY in dogs and cats
  • Irreversible changes in cartilage but also entire
    joint
  • Radiographs are specific but not sensitive
  • Treatment is mostly symptomatic and aims at minimizing progression and improving quality of life
  • A combination of lifestyle changes and treatments are often required

3. Cat & Dog 2 (50 decks)

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