Osteoarthritis Flashcards

1
Q

What part of the joint is involved in OA

A

the entire joint structure:

cartilage, subchondral bone, ligaments, menisci, synovium, and capsule

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2
Q

OA is most characterized by

A

cartilage loss

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3
Q

What is responsible for the pain in OP

A

osteophytes

**also responsible for dec ROM

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4
Q

What joints are commonly affected by OA?

A
Hip
knee
hands
spine
feet
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5
Q

what contributes most to disability in OA?

A

pain and functional limiatations

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6
Q

epidemiology of OA

A

inc with age (due to decreased cellularity of cartilage)

women > men

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7
Q

risk factors for OA

A
age
obesity
female
joint malalignment
trauma (previous surgery, fracture, etc)

also, hypermobility, osteoporosis, congenital joint dysplasia and dislocation, occupation and sport

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8
Q

What is the etiology of secondary OA

A

suboptimal repair of normal cartilage injury due to..

  1. Pre-existing joint damage (RA, gout, spondylarthritis, septic arthritis, Paget’s)
  2. Metabolic disease (Chondrocalcinosis, Hemochromatosis, Acromegaly)
  3. Systemic disease (Hemophilia, Hemaglobinopathies (sickle cell dz))
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9
Q

Pathogenesis of OA

A

mechanical stress –> release of MMPS by chondrocytes –> degradation of collagen and proteoglycans –> pro inflamm cytokines (IL-1 and TNF) are releases + NO –> increased cartilage degradation > production –> chondrocytes sense damage and attempt to repair –> repair is disordered –> hypertrophy of bone at joint margins = osteophytes –> more inflammation –> destructive cycle continues

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10
Q

in OA there is increased expression of ____ in chondrocytes

A

inducible COX 2

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11
Q

in OA ____ may contribute to the pain and predict progession of disease and need for joint replacement

A

bone marrow lesions

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12
Q

what does an osteophyte consist of?

A

fibrocartilage and bone

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13
Q

WHere are osteophyts found?

A

periph of joints at the interface of cartilage and periosteum

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14
Q

clinical presentation of OA

A

symp:

  • joint pain
  • morning stiffness (short lived
  • functional limitations

signs:

  • crepitus
  • restricted ROM
  • bony enlargements/osteophytes

(also, joint effusions, bony instability, muscle atropy)

sometimes will have elevated ESR or CRP

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15
Q

treatment goal for OA

A

Symptom relief, improve quality of life, and prevent progression of disease

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16
Q

non pharmacological treatment of OA

A

weight loss, hot/cold, exercise, orthotics

17
Q

pharmacological treatment of OA

A

topical capsaicin, NSAID, lidocane
acetaminophen, NSAIDs, narcotics
intra-articular corticosteroids and HA derivatives

18
Q

heberdons nodes vs bouchard’s nodes

A

Hep: osteophytes on DIP
Bouch: PIP

19
Q

early vs late joint changes in RA

A

early: cartilage surface irregularity and superficial clefts
late: cartilage ulceration that exposes bone

20
Q

bony changes in OA

A

due to chondocytes sensing damage and attempting to repair it –> they form clusters or cloves and cause…

sclerotic subchondral bone
hypertrophy = osteophytes
21
Q

Early and polyarticular is assc with a mutation in

A

COL2A1 gene

22
Q

deficiency in ____ is assc with OA

A

TFG-B and IGF-1

23
Q

_____ gene is assc with an increase in severity of OA

A

IL-1 receptor agonist gene