SAOP1- Osteoarthritis

  1. Articular cartilage is mostly __________, which is composed of... (4)
    hyaline; mostly water, type II collagen, proteogylcans (aggrecan**), a finite number of chondrocytes, and some other molecules
  2. Aggrecan gives cartilage the ability to...
    cushion, deform, and serves its function.
  3. What are the layers of the articular cartilage?
    • Zone I- superficial/ tangential (highest cell density, small/flat chondrocytes, parallel to joint surface)
    • Zone II- transitional (chondrocytes larger/ rounder)
    • Zone III- radial (larger chondrocytes, perpendicular to joint surface)
    • Zone IV- calcified, tidemark
  4. Describe the function of the different layers of the articular cartilage.
    • Zone I- tension parallel to surface (shear)
    • Zone II- shear and compression (smaller fibrils are parallel, larger fibrils more perpendicular)
    • Zone III- compression (fibrils are perpendicular)
  5. What are the components of the extracellular matrix and the function of each? (2)
    • type II collagen: mechanical strength, compressive stiffness, tensile strength
    • proteoglycans: (hyaluronic acid, proteins, GAGs, chondroitin sulfate, keratin sulfate) larger size, negative charge; maintains hydration of cartilage under load
  6. What are the functions of cartilage? (3)
    • low friction load bearing surface
    • moderately resistant to deformation under compression
    • with compression of joint, dynamic fluid exudation from ECM for lubrication
  7. Matrix turnover of the articular cartilage is dependent on...
    mechanical load, cytokines, growth factors, and activation of degradation enzymes [balanced by production of enzyme inhibitors and anabolic hormones]
  8. What are the order of pathological processes involved in OA as it progresses?
    • [first] cartilage pathology
    • synovial pathology
    • ligament/ tendon/ muscle pathology
    • subchondral bone pathology
    • [last] nervous system pathology
  9. The first pathological change in OA is __________, which involves...
    ECM degradation; aggrecan breakdown, collagen network disruption--> increased water content and reduced cartilage stiffness
  10. How do the chondrocytes try to compensate for ECM degradation with OA? What are the consequences of this?
    enhanced metabolic activity--> increased cartilage thickness--> chondrocyte death--> chondrocytes unable to maintain--> cartilage loss
  11. What is the origin of pain with OA?
    • synovitis and fibrosis of the synovium
    • nociceptors in the synovium, joint capsule, and subchondral bone--> inflammatory mediators sensitize nociceptors--> markedly increases input to CNS
  12. What are pathological changes of subchondral bone with OA?
    initial thinning then sclerosis and eburnation
  13. What are pathological changes of the periarticular tissues with OA? (4)
    weakness, stretching, overuse, atrophy
  14. What are the causes of arthritis? (5)
    • Non-inflammatory: traumatic, OA (primary idiopathic or secondary), neoplastic
    • Inflammatory: Immune-mediated (erosive or non-erosive), infectious
  15. What are causes of osteoarthritis? (7)
    • genetics/ developmental
    • overuse/ age
    • obesity
    • trauma
    • instability
    • immune-mediated
    • infection
  16. Why can't we use radiographs to assess loss of cartilage?
    • because we don't take standing radiographs in small animals
    • joint will look collapsed due to artifact of positioning
    • cartilage does not show up on radiography
  17. How do we diagnose OA? (3 groups of signs)
    • History and clinical signs: stiffness, lameness, inactivity, behavioral changes
    • PE: reduced ROM, creptius, pain, instability, effusion, swelling, muscle atrophy, heat
    • Radiographs: osteophytosis, enthesiophytes, effusion, periarticular swelling, subchondral sclerosis, intra-articular mineralizations, subchrondral cysts
  18. Describe joint tap findings with DJD.
    • mononuclear cells predominate
    • may have other cells of variable numbers
  19. Describe joint tap findings with septic arthritis.
    • degenerate neutrophils
    • +/- organisms (usually not.....treat as septic if you see degenerate neuts)
  20. Describe joint tap findings with IMPA.
    non-degenerate neutrophils
  21. Describe joint tap findings with neoplasia.
    unusual cells
  22. Describe the general treatment goals with OA. (8)
    • weight management****
    • nutrition- complete diet with omega-3 FAs
    • neutraceuticals- glucosamine
    • light exercise-weight loss, active ROM and muscle training
    • rehabilitation- manual therapies, strength exercises, acupuncture
    • pain meds- NSAIDs (unless immune-mediated), corticosteroids
    • structure modifying drugs- polysulfated glycosaminoglycans, pentosan polysulfate
    • +/- surgery?
  23. What are the adverse effects of NSAIDs?
    GI, hepatic, renal
  24. What pain (symptom- modifying) drugs do we use for OA? (6)
    • NSAIDs
    • Gabapentin
    • Tramadol
    • Amantadine
    • Adequan
    • Cartrophen
  25. What is the MOA of gabapentin? What are adverse effects?
    • MOA: mimics GABA, inhibits Ca flow to halt release of excitatory neurotransmitters
    • sedation, ataxis, GI side effects
  26. What is the MOA of tramadol? What are adverse effects?
    • weak mu-opioid agonist, NERI/SSRI, NDMA antagonist
    • sedation, constipation, excitation, tremors, seizures
  27. What is the MOA of amantadine? What are adverse effects?
    • antiviral, NDMA antagonist
    • GI, agitation, hepatic side effects
  28. What is the MOA of adequan?
    polysulfated glycosaminoglycan, somewhat unknown
  29. What is the MOA of Cartrophen?
    • Pentosan polysulfate
    • antithrombotic, fibrinolytic
    • may improve subchondral and synovial membrane blood flow
  30. What are surgical approaches to OA? (5)
    • joint debridement/ micropicking
    • resurfacing
    • joint replacement
    • arthrodesis (for end-stage, unable to medically manage, for comfort)
    • excision (FHO)
  31. What are the history (4) and PE (7) findings with IMPA?
    • Hx: not feeling well, weight loss, anorexia, lameness
    • PE: stiff, stilted gait, "walking on eggshells", joint effusion, pain, collapse of carpus and tarsus, lymphadenopathy, febrile
  32. How do you diagnose IMPA?
    • joint fluid tap= non-degenerate neutrophils, protein> 2.5, cells >3,000
    • rads= erosive versus no-erosive
  33. What are the 4 types of IMPA?
    • Type I: idiopathic (most common)
    • Type II: infectious or chronic inflammatory disease
    • Type III: chronic GI disease
    • Type IV: neoplasia
  34. What is the treatment for IMPA?
    • Immune suppression: prednisone, if that doesn't work--> azathioprine, cyclophosphamide, cyclosporine, lefunomide
    • Pain management: gabapentin, tramadol (NO NSAIDS!)
  35. What is the difference in joint fluid taps between DJD, septic arthritis, IMPA, and neoplasia?
    • DJD: mononuclear cells predominate +/- other cells of variable numbers
    • Septic arthritis: degenerate neutrophils +/- organism
    • IMPA: non-degenerate neutrophils
    • Neoplasia: unusual, neoplastic cells
Card Set
SAOP1- Osteoarthritis
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