2/13 Osteoarthritis Flashcards

1
Q

List the compartments of the diarthroidal joint that these disease affects:

RA

Psoriatic arthritis

Gout, pseudogout, and septic arthritis

Osteoarthritis

A

RA = synovium

Psoriatic arthritis = synovium + tendon

Gout, pseudogout, and septic arthritis = things external to the joint (urate, Calcium pyrophosphate dehydrate (CPPD), sepsis/bugs)

Osteoarthritis = cartilage (hyaline + fibrous)

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2
Q

What is the function of the hyaline/articular cartilage?

A

shock absorber of diarthroidal joints - handles 90% of load-bearing

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3
Q

What are the features of NORMAL hyaline cartilage/articular cartilage?

A

high H2O content
stiff
chondrocytes + collagen fibers distributed throughout proteoglycan matrix
interstitial fluid pressurization (like a gel-pack or sealed moist sponge)
abundant acid mucopolysaccharide (proteoglycans)

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4
Q

Is Osteoarthritis an inflammatory or non-inflammatory disease?

A

NON-inflammatory

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5
Q

What is osteoarthritis? What are other subnames of this disease?

A

progressive, symmetrical disintegration of hyaline + fibrous cartilage with secondary damage to surrounding structures

aka OA, degenerative joint disease (DJD), wear and tear arthritis

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6
Q

What is the difference between primary and secondary osteoarthritis?

A

Primary (idiopathic): very common; involves hands, spine, hips, knees, 1st MTP , et al

Secondary: precedes inflammatory disease, trauma, or metabolic factor, ie, underlying mechanical or metabolic problem such as excessive Fe in hemochromatosis, RA, ACL tear, avascular necrosis, Piaget’s disease

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7
Q

What are the lab + radiologic findings of osteoarthritis?

A

Lab:
ESR <40, RF titer <1:40, Non-inflammatory synovial fluid

Radiologic:
osteophytes (bone spurs), narrowing joint space, subchondral cysts and sclerosis, misalignment of joints

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8
Q

What are the major changes found early osteoarthritis? later?

A

Early in the disease

  • INCREASED water content, causing it to be more pliable, which results in excessive deformation, tearing, and cracking with repeated loading
  • *1. Small tangential clefts on surface** – shaggy border
  • 2. Deep vertical clefts
    3. Splitting process, “fibrillation”
    4. Clumping, hypercelluarity, and hypertrophy of chondrocytes -
    **first thing you see*
  • Reactive new subchondral bone formation
  • Extensive loss of acid mucopolysaccharide from matrix with diminished brilliant red dye fixation
  • *Later in the disease (**joints look swollen, feels like bone)
  • progressive fibrillation + loss of cartilage, resulting on bone-on-bone pathology
  • osteophyte formation & subchondral sclerosis
  • modest inflammatory infiltrates in synovium
  • ligamentous laxity, resulting in weak periarticular muscles
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9
Q

Who is the culprit of osteoarthritis?

A

chondrocytes

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10
Q

How does chondrocytes contribute to osteoarthritis?

A

Chondrocytes respond to repetitive excess mechanical loading by **promoting matrix degradation **and downregulating processes essential for cartilage repair (counter-productive!!)

proliferate + syntheseize matrix proteins/collagen, MMPs, growth factors, cytokines & other inflammatory mediators

MMPs degrade the matrix, which results in debris products in the synovial space, which further up-regulates these cellular events; ultimately result in a loss of cartilage

Anabolic factors, like BMPs & TGFb cause osteophyte formation, and chondrocyte proliferation and hypertrophy, increased cartilage calcification (tidemark duplication), & microfractures with angiogenesis from subchondral bone.

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11
Q

Osteoarthritis affects which joints in the hand the most?

knees?

A

Hands: greatest incidence in DIP + thumb base (1st carpometacarpal joint space), followed by PIP joint

  • *Knees**: greatest incidence medial compartments, but lateral and patella femoral joint is also affected
  • both medial affected = bow-legged
  • both lateral affected = knocked-knees
  • medial + lateral compartment = windswept knees
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12
Q

PIP and DIP is also known as….

A

PIP = Bouchard’s nodes
DIP = Heberden’s nodes

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13
Q

What should you think of if you see osteoarthritis in the MCP joints, especially in a young person?

A

think Hemochromatosis! (not OA)

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14
Q

Is OA more common in men or women?

A

Females:Males = 4:1; likely due to hormonal changes

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15
Q

How does obesity contribute to OA?

A

for every 10 pounds increase in weight, the force on the knee by 30-60 pounds with each step

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16
Q

What are the 4 best treatments for OA?

A
  • Weight loss
  • Exercise – improves joint stability
  • Other non-pharmacologic approaches
  • Joint replacement

When all else fails: Total Knee Replacement (TKR)

No medications has been shown to alter OA progression; only OA pain is treated