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Ortho > Osteoarthritis > Flashcards

Osteoarthritis Flashcards

1
Q

Structural classification of joints

A
  • Fibrous (e.g. skull sutures)
  • Cartilaginous (e.g. SI joint; fibrocartilage
  • Synovial (e.g. stifle; hyaline cartilage)
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2
Q

Functional classification of joints

A
  • Synarthridial (e.g. skull sutures)
  • Amphiarthridial (e.g. SI joint)
  • Diarthrodial (e.g. stifle)
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3
Q

Histology of hyaline cartilage

A
  • Chondrocytes
  • Extracellular matrix (type II collagen, PG, H2O)
  • Matrix zones: superficial (tangential), middle (transitional), deep
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4
Q

Types of forces the superficial layers works against

A
  • Shearing forces
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5
Q

Types of forces the deeper layers works against

A
  • More columnar cells and designed with type II collagen array to resist axial forces
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6
Q

Relationship between type II collagen and proteoglycan

A
  • Arches of the collagen and GAG resist axial compression
  • Type II collagen at the molecular level
  • Intimate relationship between proteoglycans (glycosaminoglycans) and the type II collagen
  • If something happens to the matrix that involves type II collagen, it will interfere with the relationship of these molecules and the function of this tissue
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7
Q

What makes up cartilage matrix?

A
  • Type II collagen and proteoglycans
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8
Q

Proteoglycan molecule structure

A
  • Core protein and glycosaminoglycans
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9
Q

How does cartilage act as a shock absorber?

A
  • When we bear weight, the cartilage is compressed
  • Water associated with proteoglycan molecules electrostatically is forced out by gravity
  • When you unload the weight on your knee, electrostatic charges are stronger than mechanical/gravitational forces, resulting in the cartilage being returned to its normal function
  • Just like a hydraulic shock
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10
Q

Pathogenesis of osteoarthritis

A
  • Something results in a disruption of the cartilage matrix and releases matrix components, which are proteoglycans, water, and chondrocytes
  • Cartilage breakdown results in cytokine cascade
  • Synoviocytes perceive inflammatory mediators and proteoglycans and enzymatic molecules
  • Synoviocytes produce interleukins, prostaglandins (pro-inflammatory mediators) to turn on their own development to produce matrix metalloproteases that go into the cartilage matrix and destroy that that more
  • Chondrocytes are stimulated to do the same thing
  • Vicious cycle
  • Degradative process
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11
Q

Chondrocytes repair potential

A
  • They don’t renew themselves that much
  • They don’t go into the “blast” stage
  • They are in such a catabolic state that they will randomly spit out proteoglycans and hyaluronic acid
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12
Q

Osteoarthritis definition

A
  • Degeneration of the articular cartilage and underlying subchondral bone
  • Also periarticular fibrosis
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13
Q

Components of osteoarthritis

A
  • Chondromalacia (death of cartilage)
  • Fibrocartilage (develops; not mechanically sound)
  • Osteophyte development
  • Synovitis (HALLMARK)***
  • Effusion (increase in water content as water is drawn into the joint osmotically)
  • Subchondral sclerosis, microfractures (cancellous bone)
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14
Q

Periarticular fibrosis

A
  • Joint capsule, ligaments, and tendons
  • Fibrous joint capsule
  • Ligaments
  • Tendons
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15
Q

What drives joint pain in osteoarthritis patients?

A
  • It is patient driven

- You treat the dog or cat

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16
Q

What can cause joint pain in certain patients with osteoarthritis?

A
  • Synovitis (inflammatory mediators)
  • Microfractures of subchondral bone (neurologic tissue)
  • Osteophytes (mechanical, depends on location)
  • Joint effusion (joint distention)***** - most common
  • OR NO PAIN
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17
Q

Which joints are more commonly clinically affected by osteoarthritis?

A
  • Front limb most often
  • Elbow
  • Carpus
  • Hock
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18
Q

% of body weight on front limb vs hind limb?

A
  • 60% BW on forelimb

- 40% BW on hindlimb

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19
Q

Why are joints in the front more commonly affected by osteoarthritis?

A
  • Biomechanics of quadriped
  • F = mass x acceleration
  • Stress and strain
  • More mass in the front
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20
Q

Primary osteoarthritis

A
  • “Wear and tear”

- Probably really “secondary” subchondral bone

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21
Q

Secondary osteoarthritis

A
  • MUCH MORE COMMON

- secondary to something else (e.g. a cranial cruciate ligament rupture or an OCD lesion)

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22
Q

Clinical causes of osteoarthritis

A
  • Hip dysplasia
  • Elbow dysplasia
  • Osteochondritis dissecans (OCD)
  • Trauma (e.g. luxation, articular fracture, septic arthritis)
  • Mechanical instability (e.g. cranial cruciate ligament rupture +- meniscal damage; subscapularis tendon rupture or medial glenohumeral ligament rupture)
  • Secondary chronic intra-articular degeneration (biceps brachii tenosynovitis
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23
Q

Diagnosis of osteoarthritis

A
  • Signalment (certain breeds; age as in more likely when older)
  • History (Lameness characteristics)
  • Physical examination
  • Imaging
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24
Q

What questions would you want to determine about the lameness?

A
  • Persistent vs intermittent
  • Activity vs rest
  • Acute vs chronic
  • Unilateral vs bilateral vs shifting
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25
Q

What to perform on a physical exam for osteoarthritis?

A
  • Gait analysis at a walk and at a trot

- Examination of the musculoskeletal system to localize

26
Q

What sorts of imaging can you do for diagnosing osteoarthritis? Which is arguably the most important?

A
  • Radiographs** (Most important)
  • Ultrasound (for muscle, tendon, or ligament)
  • CT
  • MR
  • Arthroscopy/arthrotomy
27
Q

Surgical treatment of osteoarthritis (and name which are palliative vs definitive)

A
  • Corrective osteotomy
  • Chondroplasty
  • Excisional Arthroplasty*
  • Total joint replacement*
  • Arthrodesis*
  • Amputation*
  • = definitive
28
Q

What medical treatment should ALWAYS ALWAYS ALWAYS be a part of osteoarthritis treatment?

A
  • Multimodal (AKA balanced medical management)
  • Weight reduction
  • Exercise modification (physical rehabiliation)
  • NSAIDs/DMOAs
  • +/- non-traditional, novel
29
Q

Is multimodal treatment palliative or definitive treatment?

A
  • Palliative treatment when symptomatic
30
Q

Is there a set management plan for osteoarthritis?

A
  • No
  • Individualize to each patient (e.g. is the patient overweight or not? What is the activity level of that particular patient?)
  • Tailor weight control, exercise modification, and both prescribed and nutraceutical medications to each patient
31
Q

What is arguably one of the best or most important aspects of multimodal management?

A
  • Weight reduction or control

- Reduces discomfort level, requires fewer treatments, less apt to exercise

32
Q

What are some options for weight reduction/control?

A
  • Reduce dietary intake by 1/3-1/2 per day
  • Calculations of caloric density of diet and caloric needs
  • Commercial “reducing diet” with recommended intake
  • Weight regularly/monitor with body condition score chart, or monitor for rib/waist development
33
Q

Maintenance weight strategies

A
  • Increase caloric intake with respect to activity level to maintain body weight
  • Monitor weight regularly
34
Q

What are goals of exercise in patients with OA?

A
  • Maintain strength and stamina, joint range of motion

- Less medications needed in OA patients

35
Q

What should be individualized to the patient for physical rehabilitation?

A
  • Type of activity
  • Duration and frequency of activity
  • Intensity
36
Q

Who should you see for physical rehabilitation?

A
  • Certified veterinary physical rehab specialists
37
Q

What are the pharmacologic mainstays for treatment of secondary OA?

A
  • NSAIDs
  • DMOAs (non pharmaceuticals, e.g. glucosamine, chondroitin sulfate, dietary fatty acid supplements, etc.
  • Glucocorticoids are end stage only!
38
Q

Why don’t we tend to use glucocorticoids on dogs with OA?

A
  • Can accelerate degenerative processes of articular cartilage
  • Secondary clinical effects of pharmaceutical effects on the adrenal glands
39
Q

NSAIDs - what are some examples?

A
  • Meloxicam
  • Deracoxib
  • Firocoxib
  • Carprofen
  • etc.
40
Q

What are adverse reactions of NSAIDs?

A
  • Vomiting/diarrhea (<5%)
  • Decrease appetite/anorexia (<5%)
  • Behavior change (<1% in carprofen only)
  • Hepatotoxicity - VERY rare
41
Q

How long do you want to use NSAIDs for OA?

A
  • Try not to keep on long-term NSAIDs
  • They used to, and would monitor chemistry panel every 6 months
  • Now we try to restrict them to PRN
42
Q

Hepatotoxicity of NSAIDs

A
  • VERY RARE
  • Can occur with ALL NSAIDs
  • Don’t modify the dose
43
Q

DMOA - what does it stand for?

A
  • Disease modifying osteoarthritis agents
44
Q

Examples of DMOAs

A
  • Polysulfated glycosaminoglycans
  • Nutraceuticals (Glucosamine chondroitin sulfate, avocado/soybean, MSM, fatty acid supplements, undenatured collagne type II)
  • Fish oil
  • Pentosan polysulfate
  • S-adenosyl-L-methionine
  • Methylsfulonylmethane
  • Tetracyclines
45
Q

What are polysulfated glycosaminoglycans, and how are they proposed to help OA?

A
  • Adequan injections
  • In theory and in vitro are potent anti-inflammatory medications
  • Adequan is injectable ($$$$$) but great for controlling synovitis and blocking attachment of matrix metalloproteases
46
Q

OA diets

A
  • Various diets out there
  • JD diet has a pretty significant objective improvement, but that’s mostly it
  • They contain a lot of the nutraceutical components in a convenient diet, but we don’t know how the cooking process for the food impacts those
47
Q

What type of oil can be used for OA?

A
  • FISH OIL (has probably the most evidence of working)

- Not vegetable seed oils (not absorbed welli n dogs)

48
Q

Pentosan polysulfate

A
  • Beechwood hemicellulose

- Stimulates synovial Hyaluronic acid

49
Q

S-adenosyl-L-methionine

A
  • No measurable effect based on objective measures
50
Q

Methylsulfonylmethane

A
  • Oral form of DMSO

- No impact shown on OA

51
Q

Tetracyclines and OA

A
  • Inactive metalloproteinases

- Used for more of a refractory case that isn’t surgical

52
Q

Which DMOA is considered to have the most positive clinical effects based on a meta-analysis from 2012?

A
  • Concluded that dietary fatty acid modification may have positive clinical effects (i.e. fish oil)
  • Limitation to study conclusions are that there was no identification and evaluation of “responder” groups
53
Q

What are some new treatments that are now becoming available for OA?

A
  • New Cox selective NSAIDs (cats and dogs)
  • COX/LOX Rx (tepoxalin)
  • Non-cyclooxygenase Prostaglandin E2 (PGE2) EP4 receptor antagonist (Grapiprant) that blocks formation of PGE2
  • Matrix metalloproteinase antagonists
  • Aggrecanase inhibitors (prevents breakdown of proteoglycans)
54
Q

Acupuncture for OA

A
  • No definable clinical studies that support the use for OA treatment of the elbow and hip
  • Neutralizes trigger points in myopathies
55
Q

Chiropractic treatments for OA

A
  • No controlled clinical studies
56
Q

Low level laser therapy for OA

A
  • Lacking clinical controlled studies in dogs
57
Q

Extracorporeal shock therapy for OA

A
  • Equivocal results depending on joint
58
Q

Radiation therapy for OA

A
  • Has an effect, but very short lived
59
Q

Stem cell treatment (for OA

A
  • Expensive
  • Lacking clinical controlled studies in dogs
  • Thought to be inflammatory modulation
60
Q

Platelet rich plasma for OA

A
  • Confounding clinical studies in people, horses, dogs

- Might show an improvement for 30 days

61
Q

Nutraceuticals like flavonoids, undenatured collagen II

A
  • Need clinical trials
62
Q

Can any drug reverse OA?

A
  • NO

Ortho (10 decks)

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