MS- Joints 1.txt

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  1. The synovium is richly ___________ that is formed into ________ that float within the synovial fluid.
    vascular; villi
  2. ___________ of the synovial fluid is slippery and viscous.
  3. The fibrous layer of the joint capsule provides structure to contain the...
    joint pressures within physiologic ranges
  4. The synovium is the hub of ______________.
    inflammatory mediators
  5. The articular cartilage is __________ and __________; it is designed to resist ____________ and ___________ forces.
    avascular; aneural; compressive; shear
  6. Articular cartilage is __________ cartilage.
    type II
  7. Interdigitating in the extracellular matrix is ______________ designed to resist ___________ and protect the joint from ________.
    polysulfated glycosaminoglycan; compression; loads
  8. Functions of the synovium. (3)
    make synovial fluid, add hyaluronan for lubrication of soft tissues, and connect the joint to the systemic circulation for healing and messaging
  9. The function of articular cartilage. (2)
    absorb compression and provide a tough, resilient, lo friction surface
  10. The function of subchondral bone.
    provide a hard underpinning surface that can transition the forces from cartilage to bone
  11. Joints must... (3)
    be lubricated, absorb impact, provide metabolites to articular cartilage
  12. The articular cartilage surface resists _______ and the depth resist ___________.
    shear; compression/impact
  13. The synovial membrane makes __________ plus adds ________.
    fluid dialysate of plasma; hyaluronan
  14. Subchondral bone provides resistance to ___________.
  15. Composition of the fibrous joint tissue... (2)
    type I collagen, proteoglycan
  16. Wolfe's law describes how the ______________ becomes ____________.
    subchondral bone plate; denser
  17. The articular cartilage remains turgid by harboring ____________.
  18. Repair cartilage is type _____, which is not as strong as the type ___ that was there before injury.
    I; II
  19. Component of articular cartilage that provides resistance to compression.
  20. Component of articular cartilage that provides resistance to shear.
    type II collagen
  21. _____________ are attached to the core protein in articular cartilage; the core protein attaches to ___________.
    Glycoaminoglycans (GAGs); hyaluronan
  22. Proteoglycan aggregates are turgid and therefore resist __________.
  23. What type of cartilage defects do not heal?
  24. What type of cartilage defects heal and why?
    full thickness cartilage defects because all the cartilage is gone, the bone, bleeds, and this allows healing
  25. What are 3 positive effects of exercise for joint health?
    more proteoglycan, more type II collagen, more mature repair tissue
  26. What is the subchondral bone micropik technique?
    allows improved healing of full thickness defects by allowing more blood to enter joint
  27. In remodeling, _____________ precedes ____________.
    bone resorption; bone deposition
  28. Mineralized cartilage has similar consistency to bone but lacks ___________.
    vessels (does not bleed when cut)
  29. ___________ turnover in cartilage is slight, but ____________ turnover is high.
    collagen; proteoglycan
  30. A subtle thickening and softening of cartilage due to loss of proteoglycans.
  31. In the earliest stage of chondromalacia, there is an ________ in water in the matrix; due to the increased loss of __________, water content ____________.
    increase; proteoglycans; progressively decreases
  32. With erosion, there is initially decreasing _____________ content in the cartilage, thus decreasing binding ____________, causing ___________; this cartilage is less resistant to __________, and __________ are lost.
    proteoglycans; water; degeneration; shearing; superficial layers of cartilage
  33. With fibrillation, there is continuing loss of _____________ and ____________, causing the collagen fibers in the _________ to _____________.
    matrix proteoglycans; water; radial layer; condense and split
  34. Death of chondrocytes that can be present from erosion through ulceration stages.
  35. A chondrone is an ineffectual _____________ of remaining chondrocytes.
    reactive hyperplasia
  36. Ulceration is the wearing off of cartilage to the level of the _________ or __________.
    tidemark; subchondral bone
  37. Sclerosis in the subchondral bone with its surface polished smooth due to wear in areas of ulceration.
  38. Chondro-osseous proliferation within the synovial membrane or at synovial junctions.
    osteophyte formation
  39. Osteophyte formation is likely due to... (2)
    mechanical forces due to joint instability; anabolic cytokines (TGF β)
  40. With modeling of cartilage and subchondral bone, ___________ through the ____________ will allow this layer to undergo endochondral ossification and model.
    microcracks; mineralized layer of cartilage
  41. Modeling of cartilage and subchondral bone occurs due to ________________.
    altered mechanical use
  42. ________________ may be a significant factor in joint stiffness with DJD.
    Fibrosis of joint capsule
  43. Fibrosis of the joint capsule could result in contracture due to ___________ or ____________.
    lack of use; increased fibrosis from anabolic cytokine expression (TGF β)
  44. Very early in disease due to release of sterile joint antigens.
    lymphoplasmacytic synovitis with synovial hyperplasia
  45. Bony fusion of a joint.
  46. Ankylosis across the joint space occurs by...
    direct bony fusion of ulcerated surfaces.
  47. Ankylosis around the joint space occurs due to...
    fusion of osteophyte formations at the margins of the joint.
  48. Subchondral bone cysts are cavities lined by __________ in the subchondral bone in advanced stages of ______; they are possibly secondary to the __________ of synovial fluid dissecting into subchondral bone via ______________.
    synovium; DJD; pressure; full thickness fissures in cartilage
  49. DJD is caused by anything that will injure _________ and/or reduce __________, therefore, decreasing ___________ and ___________.
    chondrocytes; proteoglycans; water; resistance to wear
  50. 3 causes of DJD.
    aging chondrocytes, injury to synovial cells/chondrocytes, subchondral bone sclerosis
  51. Aging chondrocytes can cause DJD because...
    they have decreased proteoglycan synthesis.
  52. Injury to synovial cells/chondrocytes causes ________, which induced increased __(3)__; these substances decrease __________ synthesis and activate __________, causing DJD.
    inflammation; IL-1, TNF, prostaglandins; proteoglycan synthesis; MMPs
  53. Proteolytic enzymes that catabolize matrix collagen and proteoglycans.
    metalloproteinases (MMPs)
  54. A common sequela to DJD due to the loss of cartilage and reduced buffering of impact forces on bone; compensatory.
    subchondral bone sclerosis
  55. Inflammation often with associated degeneration, necrosis, lysis, and attempts at repair of articular cartilage, synovium, joint capsule, and adjacent bone due to infection.
    infectious inflammation of joints
  56. 3 causes of infectious inflammation of joints.
    bacteria, mycoplasma (LA), viruses
  57. 2 viruses known to cause infectious inflammation of joints.
    CAEV in goat, reovirus in poultry
  58. 4 routes of entry for infectious inflammation of joints.
    hematogenous, subchondral osteomyelitis, physitis, traumatic innoculation
  59. Subchondral osteomyelitits can cause infectious inflammation of joints because the exudates can cause ________ of the ____________, eventually extending into the joint.
    lysis; overlying layers of mineralized and unmineralized articular cartilage
  60. Physitis can cause infectious inflammation of joints because the exudate can break through the _________ at the ____________, where compact bone has not yet formed.
    cortex; periphery of the physis
  61. Infectious inflammation of joints is caused by bacteria because they have _________, they produce ________, and/or they have ___________ that activate host cells.
    toxins; lytic enzymes; membrane proteins
  62. Host factors that can contribute to infectious inflammation of joints. (3)
    humeral factors (cytokines), inflammatory cells, necrotic/degenerate/reactive structural cells
  63. Necrosis/degeneration of chondrocytes can contribute to infectious inflammation of joints because there is failure to maintain _____________ and ________ of the matrix, leading to ___________.
    proteoglycans; collagen; enzymatic destruction
  64. Necrosis/degeneration of synoviocytes can contribute to infectious inflammation of joints because there is failure to ________________, causing injury to _________.
    lubricate and nourish cartilage; chondrocytes
  65. Fibroblasts in reactive synovial tissue can ______________ to produce _________ that are lytic to cartilage; does NOT occur in DJD, only infectious inflammation of joints.
    grow into articular cartilage (pannus formation); MMPs
  66. Infectious inflammation of joints can lead to _________; synovial damage leads to decreased _________ and _________; incongruous surfaces lead to decreased ___________ and __________; loss of chondrocytes leads to inadequate _________ and activation of _________.
    DJD; nutrition; lubrication; nutrition; lubrication; proteoglycan synthesis; MMPs
  67. Acute structural changes associated with infectious inflammation of joints. (2)
    fibrinous and neutrophilic exudate, decreased viscosity of fluid
  68. Subacute structural changes associated with infectious inflammation of joints. (3)
    exudate in synovial fluid and synovium, synovial hyperplasia, lymphoplasmacytic synovitis [no cartilage loss]
  69. Chronic structural changes associated with infectious inflammation of joints. (6)
    exudate, erosion, ulceration of articular cartilage, pannus formation, osteophyte formation, ankylosis
  70. 3 specific types of chronic infectious inflammation of joints.
    chronic fibrinous arthritis, chronic suppurative arthritis, chronic fibrinopurulent arthritis
  71. Fibrovascular repair tissue arising from the synovial membrane that grows onto and can invade the articular surface; may grow between the articular cartilage and the underlying bone.
    pannus formation
  72. Pannus formation tends to occur with _____________.
    chronic fibrinous arthritis
  73. Non-infectious inflammation of joints due to an autoimmune reaction against self-antigen.
    rheumatoid arthritis (often associated with SLE)
  74. How can residual bacterial peptidoglycans cause non-infectious inflammation of joints?
    remain in joint after infection is gone and act as persistent antigen
  75. Non-infectious arthritis that occurs within one month of a primary infection elsewhere in the body (ie. not a joint).
    reactive arthritis
  76. 3 theories for the pathogenesis of reactive arthritis.
    localization of antigenic bacterial peptidoglycans in joints; homing to joints of lymphocytes sensitized at other sites of inflammation; mimicry b/w bacterial Ag and host histocompatibility Ag
  77. 2 possible causes of immune-mediated polyarthritis in dogs.
    idiopathic; associated with infectious GI disease and neoplasia
  78. 2 types of erosive non-infectious inflammation of joints.
    rheumatoid arthritis, reactive arthritis
  79. Erosive non-infectious inflammation of joints has similar lesions to ___________.
    chronic fibrinous arthritis (pannus)
  80. 2 types of non-erosive non-infectious inflammation of joints.
    SLE, immune-mediated polyarthritis of dogs
  81. Non-erosive non-infectious inflammation of joints has lesions similar to those of _____________.
    acute to subacute neutrophilic arthritis
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MS- Joints 1.txt
2015-04-14 20:42:47
vetmed joints

vetmed, joints part 1
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