Osteoarthritis Flashcards

(32 cards)

1
Q

What is osteoarthritis?

A

Joint failure/pathologic changes in all joint structures with hyaline articular cartilage loss, thickening/sclerosis of bony plates, outgrowth of osteophytes at joint margins, articular capsule stretching, mild synovitis, and weakness in muscles bridging joints

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2
Q

What are systemic risk factors for OA?

A

Older age, female sex, genetic factors, excess body weight, certain occupations, elite athletic activity

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3
Q

What are local risk factors for OA?

A

Major injury, meniscectomy, developmental abnormalities, varus alignment, meniscal tear/meniscal extrusion

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4
Q

What are occupational risk factors for OA?

A

Knee - heavy lifting, mining
Hip - farming
Elbow - jackhammer operator
Hand - cotton mill

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5
Q

What is the natural history of OA?

A

Some joints will not progress, others will have phases of compensation (remodeling) and decompensation (more insult than repair)

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6
Q

What are the constituents of healthy cartilage type II?

A
  • type II cartilage collagen fibrils
  • aggrecan
  • ECM proteins
  • chondrocytes
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7
Q

What is the function of aggrecans?

A

Proteoglycans that link with hyaluronic acid and retain water to give cartilage compressive stiffness

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8
Q

What is the function of chondrocytes?

A

Cartilage cells that synthesize elements of the matrix, produce cytokines/growth factors/enzymes

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9
Q

What are the main proteinases involved in cartilage destruction of OA?

A

Matrix metalloproteinases

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10
Q

What controls the function of MMPs?

A

TIMPs (tissue inhibitors of MMPs)

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11
Q

What are the stages of cartilage pathology in OA?

A

surface fibrillation and irregularity –> full-thickness defect to the bone –> cartilage damage/loss to bare bone

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12
Q

What pathological changes occur in bones in OA?

A

Thickening/stiffening of subchondral plate and osteocyte formation in joint margins

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13
Q

What pathological changes occur in the synovium in OA?

A

Can become edematous and inflamed (but not as much as inflammatory joint pains)

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14
Q

What pathological changes occur int he joint capsule in OA?

A

Edema, later fibrosis

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15
Q

What is phase 1 of OA?

A
  • edema of ECM
  • microcracks on cartilage
  • focal loss of chondrocytes, alternating with areas of proliferation
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16
Q

What is phase 2 of OA?

A
  • microcracks deepen
  • vertical clefts form in cartilage
  • clusters of chondrocytes appear around these clefts and at surface
17
Q

What is phase 3 of OA?

A
  • fissures cause cartilage fragments to break off (osteocartilaginous loose bodies)
  • subchondral bone uncovered
  • subchondral cysts
  • mild synovitis
  • subchondral bone sclerosis
18
Q

What sites are commonly affected by primary OA?

A
Hands (DIP, PIP, first CMC)
Cervical and lumbar spine
Feet (especially 1st MTP big toe)
Knees (medial or lateral tibiofemoral compartment not both)
Hips
C and L spine
19
Q

What joint involvement pattern is suggestive of generalized OA?

A

Hands + at least one large joint

20
Q

What are Heberden’s nodes?

A

Enlarged DIP joints, common in generalized OA

21
Q

What are symptoms of early OA?

A

aching pain that increases with joint use and is relieved by rest

22
Q

What are symptoms of advanced OA?

A

aching pain at rest and with use, night pains, sleep interference worsens pain

23
Q

What are key physical exam findings of OA?

A
  • bony enlargements at joints
  • limited motion
  • crepitus (crackling)
  • malalignment
  • mild inflammation, warmth, and effusion
24
Q

What are bouchard’s nodes?

A

Swelling at the proximal interphalangeal (PIP) joints

25
What are the common synovial fluid findings of OA?
non-inflammatory fluid, low turbidity, low WBC, may have pseudogout crystals
26
What are radiographic findings associated with OA?
- focal joint space narrowing, often asymmetric - marginal and central osteophytes - subchondral sclerosis and cysts - osteochondral bodies - bony attrition
27
Which imaging modality is most useful for evaluation of OA?
X-rays, MRIs are mostly used in research and do not demonstrate findings that would alter management
28
What factors are associated with progression of knee OA?
Excess body weight, varus alignment (bow-legged), valgus alignment (knock-knee), meniscal damage
29
What are the non-pharmacologic treatments of OA?
- education on coping strategies and self-efficacy - physical and occupational therapy - weight loss
30
What are systemic pharmacologic treatments of OA?
- non-narcotic analgesics (acetaminophen) - anti-inflammatories (NSAIDs, COX-2 inhibitors) - narcotic analgesics
31
What are local pharmacologic treatments of OA?
- intra-articular injections - corticosteroids - hyaluronic acid (low evidence)
32
What are disease-modifying pharmacologics for OA?
There aren't any