Lecture 12: Equine Osteoarthritis Flashcards

1
Q

Where are the nerve endings in a joint capsule

A

Fibrous joint capsule

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2
Q

What does a flexion test do

A

Puts stress on fibrous joint capsule, aggregates nerves and can make lame limb more obvious

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3
Q

What is synovial fluid

A

Ultrafiltrate of plasma and secretions

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4
Q

What is the intima of synovial fluid

A

Made of synovial cells that act as a filter of what is going in and out of joint capsule

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5
Q

What does the subintima contain

A

Ground substance/ glycoaminoglycosides (GAG)

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6
Q

How does synovial effusion occur when joint swells

A

Intima space gets bigger and fluid leaks in faster than it can get removed

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7
Q

What is the appearance of normal synovial fluid

A

Vicious

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8
Q

What is the cell count of normal synovial fluid

A

<500/ul

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9
Q

What % do lymphocytes, monocytes and synovial lining cells make up for normal synovial fluid

A

90%

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10
Q

Neutrophils make up __% of normal synovial fluid

A

10%

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11
Q

Is there endogenous hyaluronic acid

A

Yes, 0.5mg/ml

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12
Q

T or F: synovial fluid clots

A

False, no clot no fibrin, unless swollen then fibrin will leak in

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13
Q

What layer maintains the tensile strength in the articular hyaline cartilage

A

Tangential layer

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14
Q

What layer of the articular hyaline cartilage maintains the cyclic deformation/squish

A

Radial layer

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15
Q

Healing of the joint/articular hyaline cartilage requires removal of what layer

A

Calcified cartilage

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16
Q

What makes up the ground substance

A

Glycoaminoglycans (GAGs) and proteoglycans

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17
Q

What type of strength do the more superficial layers of articular cartilage provide

A

Tensile strength

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18
Q

What type of strength do the deeper layers of articular cartilage provide

A

Compressive, stiffness (squish)

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19
Q

Describe the joint lubrication for low loads

A

Boundary lubrication from hyaluranon and lubricin- decreases friction

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20
Q

What structures provide joint lubrication for low loads

A

Synovial membrane, synovium-cartilage, cartilage-cartilage

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21
Q

Describe the joint lubrication at high loads

A

Hydrostatic (squeeze film) lubrication of cartilage-cartilage interface

Fluid will extrude from cartilage surface to go between cartilage surfaces and then fluid goes back in (why we need squish)

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22
Q

What provides structural support and is the primary shock absorber- protects articular cartilage

A

Subchondral bone

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23
Q

___takes away cushion and cartilage in damaged in subchodnral bone

A

Sclerosis

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24
Q

What are some inciting causes of DJD

A
  1. Direct injury
  2. Biochemical- inflammation, sepsis, iatrogenic (steroids)
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25
Q

What happens to cartilage in DJD

A

Loss of proteoglycans, becomes weaker, fibrillates and cracks, ground substance disappears

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26
Q

What is the end result of DJD

A

Osteoarthritis

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27
Q

How does OA appear on radiographs

A
  1. Narrowing of joint space
  2. Subchondral bone and periarticular changes- sclerosis, lysis/cystic lesions, periarticular osteophyte formation
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28
Q

Identify which is normal and which has DJD

A

Left: DJD, narrowing
Right: normal

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29
Q

Identify the general problem and then issues indicated by 1-3

A

OA- ringbone (high at pastern joint)
1. Joint narrowing
2. Subchondral sclerosis
3. Lysis

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30
Q

Identify the problem and where is it

A

Distal Tarsal OA (Bone spavin)
Loss of joint space, Subchondral bone sclerosis/lysis

31
Q

What are some factors in DJD for abnormal stresses on normal cartilage

A
  1. Chondral/ osteochodnral injury
  2. Joint instability (collateral ligament tears)
  3. Steroid (MPA) injections
32
Q

What are some factors in DJD that are normal stresses on abnormal cartilage

A
  1. Synovitis
  2. Capsulitis
  3. Osteochondrosis
33
Q

what is wrong

A

P1 fracture

34
Q

What is wrong and how can this contribute to OA

A

Collateral ligament tear- causing joint instability

35
Q

What is wrong and how can this contribute to OA

A

Space where arrow is pointing is too big between carpal and intermediate carpal bones

Leads to joint instability

36
Q

What is wrong here and what can it lead to that will contribute to OA

A

Distal tibial OCD- leading to synovitis

37
Q

OCD is a very common cause of ___

A

Synovitis

38
Q

What is wrong here and what can it lead to that contributes to OA

A

Chip fracture at P1- bone fragment will wiggle and create inflammation—> synovitis

39
Q

What are the main players in synovial inflammation

A
  1. Synovial cell
  2. Chondrocytes
  3. PMN (especially with sepsis)
40
Q

Which is normal vs abnormal, what is wrong. And use of what could have caused this?

A

Left: normal
Right: GAG loss due to steroids (Mehthylprednisolone acetate/ MPA

41
Q

What is wrong here

A

cartilage fibrillation

42
Q

What is wrong here

A

erosion of shoulder joint

43
Q

T or F: limited capacity to repair articular cartilage in adults

A

True

44
Q

T or F: hyaline cartilage can be replaced

A

False

45
Q

What is hyaline cartilage replaced with

A

Cartilage defect granulation/ fibrous tissue fibrocartilage

Type 1 collagen (not as good as type 2)

46
Q

What does this show

A

Fibrocartilage, due to repair from injury of articular cartilage

47
Q

Fibrocartilage is important in repair of damage to joint/ articular cartilage because it…..

A

Seals the defect and stops the inflammation

48
Q

Image on left had defect cartilage removed to expose ___ indicated by yellow arrow

A

Subchondral bone

49
Q

How do you manage joint inflammation

A
  1. Prevention- conformation, foot care
  2. Exercise management
  3. Weight loss
50
Q

What are the systemic medical management options for osteoarthritis

A
  1. NSAIDs- phenylbutazone, banamine
  2. Glucosamine
  3. DSMO IV
  4. Hyaluronic acid IV
  5. Polysulfated glycosamingolycans (adequan)
51
Q

How do NSAIDS decrease inflammation

A

Inhibit arachidonic acid pathway by inhibiting COX

52
Q

Corticosteroids can be used intra-articularly but cause ___depletion over time

A

GAG

53
Q

What is the drug of choice for intra-articular steroids

A

Triamcinolone acetonide

54
Q

How does triamcinolone acetonide work

A

Inhibit PLA2 in arachodonic acid pathway and suppresses inflammation

55
Q

What is the maximum dose for traimcinolone per horse

A

18mg/horse

56
Q

Steroid induce __can be observed with exceeding maximum

A

Laminitis

57
Q

What steroid has significant GAG depletion

A

Methylprednisolone acetate (MPA)

58
Q

MPA should not be used in what joints

A

High motion joints

59
Q

___acid does not mitigate negative effects of MPA

A

Hyaluronic acid

60
Q

Hyaluronic acid with ___or ___ does have chondroprotective effect

A

Triamcinolone and betamethasone

61
Q

___with MPA is very harmful to cartilage

A

Lidocaine

62
Q

What does hyaluronic acid do in joint

A

Anti-inflammatory
Steric hinderance of particles through synovium/ mesh filter/ intima

63
Q

T or F: hyaluronic acid has negative effects on cartilage

A

False

64
Q

What do polysulfated glycoaminoglycans (adequan) do in tx of joints

A
  1. Stimulate endogenous hyaluronic acid
  2. Increase proteoglycans and collagen synthesis by chondrocytes
  3. Inhibit metalloproteases
65
Q

Intra-articular use of adequan must be given with ___because it potentiates joint infections

A

Amikacin

66
Q

What is the mechanism of action of IRAP

A

Blocks IL-1

67
Q

IRAP is made from

A

Horses own blood

68
Q

T or F: IRAP has negative effects

A

False

69
Q

PRP has ___proteins

A

Potent anti-inflammatory proteins

70
Q

PRP is used more for __injuries

A

Ligament

71
Q

PRP can cause post injection ___

A

Flare

72
Q

What is post injection flare

A

Acute swelling/effusion and lameness immediate post injection to 24-48hrs

Chemical reaction to whatever you injected

73
Q

What do you do for post injection flare

A

If continues to worsen 24-48hrs after injection lavage joint, put on hyaluronic acid and no steroids