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Flashcards in Osteoarthritis Deck (32)
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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

2
Q

What are systemic risk factors for OA?

A

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

3
Q

What are local risk factors for OA?

A

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

4
Q

What are occupational risk factors for OA?

A

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

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)

6
Q

What are the constituents of healthy cartilage type II?

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

What is the function of aggrecans?

A

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

8
Q

What is the function of chondrocytes?

A

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

9
Q

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

A

Matrix metalloproteinases

10
Q

What controls the function of MMPs?

A

TIMPs (tissue inhibitors of MMPs)

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

12
Q

What pathological changes occur in bones in OA?

A

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

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)

14
Q

What pathological changes occur int he joint capsule in OA?

A

Edema, later fibrosis

15
Q

What is phase 1 of OA?

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

What are the common synovial fluid findings of OA?

A

non-inflammatory fluid, low turbidity, low WBC, may have pseudogout crystals

26
Q

What are radiographic findings associated with OA?

A
  • focal joint space narrowing, often asymmetric
  • marginal and central osteophytes
  • subchondral sclerosis and cysts
  • osteochondral bodies
  • bony attrition
27
Q

Which imaging modality is most useful for evaluation of OA?

A

X-rays, MRIs are mostly used in research and do not demonstrate findings that would alter management

28
Q

What factors are associated with progression of knee OA?

A

Excess body weight, varus alignment (bow-legged), valgus alignment (knock-knee), meniscal damage

29
Q

What are the non-pharmacologic treatments of OA?

A
  • education on coping strategies and self-efficacy
  • physical and occupational therapy
  • weight loss
30
Q

What are systemic pharmacologic treatments of OA?

A
  • non-narcotic analgesics (acetaminophen)
  • anti-inflammatories (NSAIDs, COX-2 inhibitors)
  • narcotic analgesics
31
Q

What are local pharmacologic treatments of OA?

A
  • intra-articular injections
  • corticosteroids
  • hyaluronic acid (low evidence)
32
Q

What are disease-modifying pharmacologics for OA?

A

There aren’t any