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Musculoskeletal > Osteoarthritis > Flashcards

Osteoarthritis Flashcards

1
Q

T/F: osteoarthritis is characterized by extensive inflammation

A

False; non-inflammatory disease

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2
Q

What is the preogression of osteoarthritis?

A 
Chondromalacia
Surface fibrillation
Fissuring
Calcification
Eburnation
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3
Q

What happens at the articular margins during the progression of psteoarthritis?

A

Osteophytosis

Chip fractures

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4
Q

What happens in the synovial capsule during the progression of psteoarthritis?

A

Fibrosis

Enthesiophytosis

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5
Q

What happens to the subchondral bone during the progression of osteoarthritis?

A

Sclerosis (thickening)

Lysis

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6
Q

What are the cellular zones of articular cartilage?

A 
Superficial
Middle (radial)
Deep
Calcified
Subchondral
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7
Q

What is the purpose of the collagen type II arcuate network?

A

Keeps cartilage from swelling beyond constraints

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8
Q

What happens to chondrocytes as animals age?

A

Chondrocytes diminish and the area the remaining cells have to cover gets larger, so they get larger

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9
Q

Why aren’t there any signs of inflammation with degeneration of articular cartilage?

A

Avascular (no heat/redness)
Alymphatic (no swelling)
Aneural (no pain)

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10
Q

In the most basic terms, what leads to OA?

A

Persistent imbalance between catabolic and anabolic activities

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11
Q

What are some possibilities for pathogenesis of OA?

A

Hip and elbow dysplasia
Aseptic necrosis
OCD variants

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12
Q

What are some pathogeneses of secondary OA?

A 
Conformational abnormalities
Primary soft tissue lesions
Developmental diseases
Excessive loading
Trauma/intra-articular fxs
Infection
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13
Q

How do conformational abnormalities predispose to OA?

A

Excessive loading across joint surfaces

Excessive compressive forces damage cartilage and lead to irreversible changes

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14
Q

Define post-traumatic OA

A

Immediate chondrocyte death with fx
Progressive cell death and matrix destruction with instability
Variable ongoing degeneration, based on the quality of repair

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15
Q

T/F: OA is usually a primary condition

A

False; usually a secondary consequence of primary condition

Treatment of initiating cause often prevents or slows progression

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16
Q

What are the mediators of OA?

A 
Interleukins 1a and b
- MMP activity and PgE2 production
- IL 6, plasminogen activator, iNOS
- Proteoglycan and collagen synthesis
TNFalpha
- IL-1 and IL-6 expression
-Proteoglycan and collagen synthesis
PgE2
- Stimulates vasodilation and pain
- Proteoglycan synthesis
- Proteoglycan degredation
17
Q

What are some effectors of matrix breakdown?

A 
Primary mechanical disruption
Matrix metalloproteinases (MMPs 2, 3, 9, 13)
Collagenases 1 and 3 (collagens)
Stromelysin 1 (aggrecan, link protein, collagens)
Gelatinase (collagen type II)
18
Q

T/F: MMPs require Zn for catalytic activity

A

True

19
Q

T/F: MMPs require proteolytic activation (by cathepsins, plasmin, stromelysin, etc)

A

True

20
Q

T/F: MMPs are antagonized by TIMPs

A

True

21
Q

What are aggrecanases?

A

A disintegrin and metalloproteinase with thrombospondin motifs

22
Q

What are cathepsins?

A

Acidic lysosomal serine proteases

Activate proenzymes, degrade pericellular GAGs

23
Q

What do free O radicals do?

A

Degrade synovial hyaluonan

24
Q

What are the stages of OA cartilage pathology?

A

Matrix depletion
Proteoglycan loss
Surface fibrillation
Chondrocyte loss

25
Q

What are osteophytes?

A

Small growths of bone

26
Q

How does OA bone appear on pathology?

A

Increased trabecular bone volume
Increased distance between trabeculae
Fewer, thicker trabeculae
Slab fractures follow pathological sclerosis and cumulative microtrauma to the trabeculae that exceed the reparative capacities of the tissue

Reduced biomechanical function
“Brittleness” = predisposition to fracture

27
Q

What is ankylosis?

A

stiffening of a joint due to fusing of the bones

28
Q

On CT, how does bone edema appear?

A

Bright white areas around bone

29
Q

What is synovial hyperplasia?

A

Thickening of the synovium by several cell layers (should be 2-3 cells thick)

30
Q

What are the clinical signs of OA?

A

Mild but progressive lameness
Animals often “warm out” of lameness with work
Variable joint effusion and capsular thickening, resulting in reduced range of motion and pain on flexion
Synovial fluid changes are often unremarkable
“High incidence” joint involvement

Musculoskeletal (7 decks)

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