Tuesday: Osteoarthritis Flashcards

1
Q

Osteoarthritis: What is it?

A

Alterations in joint architecture secondary to cartilage degeneration together with somewhat misdirected bone and cartilage regrowth.

Degenerative joint disease and osteoarthritis=marked inflammation is not prerequisite for articular destruction of osteoarthritis.

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2
Q

Secondary osteoarthritis is…

A

Caused by pre-existing condition that has adversely affected joint.

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3
Q

Who gets osteoarthritis?

A

Over age 65
Men and women equal.

Primary generalized osteoarthritis if found more frequently in women and displays familial aggregation. This type involves DIP (Heberden’s nodes).

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4
Q

Pathology of osteoarthritis?

A

Gradual destruction and attempted regeneration.

Early in disease: Articular cartilage loses glistening appearance. Surface layers wear away and still later fissures develop that are perpendicular to joint surface. Ability of cartilage to withstand pressures of normal use is reduced.

Changes are worst on load bearing surfaces: Cartilage becomes thin and exposes underlying subchondral bone that becomes thicker.

Cysts may form in subchondral bone. Cysts that are usually less than 1 cm in diameter and are rimmed by sclerotic bone. Some cysts communicate with fissures in overlying cartilage. Others are filled with fibromyxoid degenerative tissue.

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5
Q

Spur-like outgrowths develop at edges of osteoarthrtitic joints. How do these form?

A

Begin as proliferation of marginal articular cartilage, deeper layers are invaded by new blood vessels and form bone via enchondral ossification. This is attempt to increase load bearing surface of joint.

Hyaline cartilage forms not articular.

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6
Q

Joint mice?

A

Spurs break off and become free intra articular fragments know as joint mice.

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7
Q

In osteoarthritic joints,

deeper chondrocytes demonstrate proliferation in clusters referred to as…

A

Clones or brood capsules

This is attempt at cartilage repair.

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8
Q

Pathogenesis of osteoarthritis

A

Chronic trauma, joint incongruities, malalignment, genetic and metabolic factors play roles.

MAIN IDEA: DEFECTS IN NORMAL MATRIX SYNTHESIS AND ALTERATIONS IN NORMAL DEGRADATION PROCESS.

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9
Q

Alterations of molecules in osteoarthritis:

A

Aggrecan (resulting in shorter molecule and smaller side chain) can impair water holding properties of cartilage.

Synthesis of Type I rather than Type II collagen.

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10
Q

Typical presentation of primary generalized osteoarthritis.

A

Women in 5th or 6th decade. Gradual onset of pain in DIP joints. Nocturnal fingertip pain and paresthesia may develop.

Cystic swellings of hyaluronic acid on dorsolateral aspects of joints. Excrescences of bone and cartilage at DIP joints=Heberden’s nodes.

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11
Q

Inflammatory osteoarthritis: Presentation

A

Painful erythema of one or more DIP joints (mimicking acute inflammatory disorder)

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