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Rheum/Musculoskeletal/Derm Week 1 > Osteoarthritis > Flashcards

Osteoarthritis Flashcards

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Dermatology Board Prep flashcards
1
Q

T or F. Rheumatoid arthritis never involves the DIP joints in the hand

A

T. Only the PIP and MCP

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2
Q

What is osteoarthritis?

A

a degenerative (not very inflammatory-some though) joint disease occurring primarily in older individuals, characterized by erosion of the articular cartilage, hypertrophy of bone at the margins (i.e. osteophytes-seen on x-ray), and subchondral sclerosis (more white!)

synovial is not really enlarged like in RA

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3
Q

What are some risk factors for developing osteoarthritis?

A

age, joint location, obesity (adipocin elevation promotes degradation!), genetic predisposition (will present younger-40~), trauma, and female

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4
Q

What are some morphologic changes in early osteroarthritis?

A

articular cartilage surface irregularity, superficial clefts within tissue, and altered /decreased proteoglycan distribution

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5
Q

What are some morphologic changes in late osteroarthritis?

A
  • deepened clefts with more surface irregularities

- eventual articular cartilage ulceration, exposing underlying bone

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6
Q

What causes secondary osteoarthritis?

A

a suboptimal repair response of normal articular cartilage to injury

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7
Q

What are some mediators classically associated with the low-grade inflammation during osteoarthritis?

A

IL-1B and TNFa (inhibiting these makes the patient susceptible to infection or autoimmune disease)

biologics aren’t usually used because the disease process takes so long

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8
Q

What is a major molecule produced by chondrocytes in response to pro inflammatory cytokines?

A

NO (and PGE2)

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9
Q

T or F. Expression of inducible COX-2 is increased in osteoarthritis chondrocytes

A

T.

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10
Q

T or F. Subchondral sclerosis is seen in osteoarthritis

A

T.

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11
Q

What is responsible for degrading proteoglycans?

A

metalloproteinases (aggrecanases)

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12
Q

Big difference between osteoarthritis and rheumatoid arthritis?

A

joint damage occurs over several decades in osteoarthritis whereas it is very fast in rheumatoid arthritis

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13
Q

Pathologic mechanism of osteoarthritis

A

Mechanical stress initiates altered metabolism characterized by the release of matrix metalloproteinases (MMPs)-activated by plasminogen activator-, proinflammatory cytokines, and mediators such as NO and PGE2.

Cartilage breakdown products play a role by stimulating the release of cytokines from synovial lining cells and by inducing MMP production by chondrocytes.

Perpetuation of cartilage damage is amplified by the autocrine and paracrine actions of interleukin (IL)-1β and TNF produced by chondrocytes.

NOTE: TGF-B can be produced and is protective to cartilage by inhibiting MMPs

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14
Q

How does OA present?

A

pain is related to use and usually gets worse during the day, when range of motion decreases

keep in mind that in rheumatoid arthritis, pain will typically get BETTER with joint use

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15
Q

Is morning stiffness evident in OA?

A

yes, but only for around 20-30 min (also commonly after inactivity = aka gelling)

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16
Q

What other clinical things may be seen with OA?

A
  • Joint instability
  • Bony enlargement (not seen in rheumatoid arthritis)
  • Restricted movement
  • Crepitus (made by rubbing of cartilage clefts)
  • Variable swelling and/or instability
17
Q

What percentage of people over age 70 have OA?

A

75%

18
Q

What joints are typically affected by primary OA?

A
  • hips and knees
  • big toe (MTP)
  • whole cervical and LS (lumbosacral) spine (not thoracic)- see osteophytes that can impinge nerves
  • MCP in the thumb
  • DIP and PIP in digits 2-5

carpal bones, ankle, elbow, and shoulder- think secondary

19
Q

Radiologic features of OA

A
  • Joint space narrowing
  • Marginal osteophytes
  • Subchondral cysts
  • Bony sclerosis
  • Malalignment
20
Q

Characteristics of OA in synovial fluid

A

less than 200/mm^3 leukocytes (may be a little higher) with less then 25% PMNs

more PMNs= infected joint

21
Q

OA in the ankle is not usually seen unless what co-mordibities are present?

A

hemochromatosis or severe obesity

22
Q

Jobs common with OA?

A

jackhammer worker and mechanics may have extensive OA

23
Q

Other disorders associated with OA?

A

syphilis and diabetes- lose proprioception (knee most commonly involved)

24
Q

T or F. The spine is not involved in rheumatoid arthritis

A

T. Except maybe C1-C3 but is involved in OA

25
Q

Other signs of OA?

A

Heberden’s (via increased pericondrium activity) and Bouchard’s nodes and squaring at the base of both thumbs

26
Q

T or F. The ulnar styloid is eroded in OA

A

F. Only eroded in rheumatoid arthritis

27
Q

Metabolic diseases associated with OA?

A
  • hemochromatosis
  • hyperPTH
  • hypothyroidism /magnesemia/phosphatasia
28
Q

First line DOC for OA? Main toxicity? Max safe dose?

A

acetaminophen (beware toxicity form use of multiple OTC drugs)- main toxicity is the liver

max safe dose- 4 gm/day

29
Q

Other therapy options?

A

intra-articular steroids every 3 months to remove fluid and provide pain relief, or

hyaluronate injections (limited to knees) to allow time to lose weight before replacement of joint

30
Q

Risks with intra-articular steroids?

A

risk infection or worsening of diabetes mellitus or CHF

31
Q

What type of collagen is found in a joint?

A

Type II- three strands of a1 (susceptible to collagenases cutting at 1/3rd length)

32
Q

T or F. SED is elevated in OA

A

F.

33
Q

Management of OA

A
  • Advice exercise to the point of pain to strengthen the muscles around the joint
  • Decrease pain to increase function (acetaminophen)
  • Hot/cold packs
  • Weight loss

make sure the pain is joint related (not a tendonitis or bursitis adjacent to joint)

34
Q

Pharm managments of OA

A
  • High dose Acetaminophen
  • Intra-articular agents

NSAIDs and opioids IF NEEDED

35
Q

Surgical therapy for OA?

A
  • Arthroscopy
  • Osteotomy (may delay need for TKR for 2-3 yrs)
  • TKR as last resort

Rheum/Musculoskeletal/Derm Week 1 (25 decks)

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