OA Flashcards

0
Q

What are the risk factors for OA?

A
  • obesity
  • occupation, sports, trauma
  • genetics, age, gender (non-modifiable)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

What is the prevalence of osteoporosis in Canadians?

A

1 in 10 (3 million)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Why are females more likely to get OA?

A
  • because of pregnancy

- babies suck the calcium out of the bones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What joints are affected from most to least?

A
  • spine
  • hip
  • hand
  • knee
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What systemic factors affect joint vulnerability contribute to OA progression?

A
  • increased age
  • female gender
  • racial/ethnic factors
  • genetic susceptibility
  • nutritional factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are some intrinsic joint vulnerabilities that can contribute to OA?

A
  • previous damage
  • bridging muscle weakness
  • increasing bone density
  • malalignment
  • proprioceptive deficiencies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is primary OA?

A
  • idiopathic cause
  • localized OA = 1-2 joints affected
  • generalized OA = 3+ joint affected
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is secondary OA?

A
  • known cause
  • RA
  • trauma
  • disease
  • obesity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Cartilage is made by ______________.

A

chondrocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the 2 macromolecules made by chondrocytes?

A

Type II collagen - provides tensile strength

Aggrecan - negatively change glycosamioglycans

  • blocks the inactive DDR-2 receptor
  • electrostatic repulsion gives cartilage in compressive stiffness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the degrading enzymes produced by chondrocytes?

A

Matrix metalloproteinases 13 - breaks down type II collagen

ADAMTS 4 and 5 - break down aggrecan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

We used to think that OA was just a “wear and tear” disease.
We now know:

A
  1. mechanical wear/trauma acts as catalyst starting disease process
  2. actually cartilage damage is a chemically-mediated disease process
  3. complex cellular mechanisms cause increase catabolic and stunted anabolic mechanisms of cartilage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe the cartilage breakdown cycle in OA.

A
  1. Cartilage damage stimulates chondrocytes activity
  2. Chondrocytes produce ADAMTS-5 which breaks down aggrecan
  3. DDR-2 receptor is now exposed and activates MMP-13
  4. MMP-13 and activated DDR-2 begins destroying collagen
  5. Destruction of collagen signals for more ADAMTS-5 to be made
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Will increased levels of MMP-13 destroy collagen?

A

No, not unless the DDR-2 receptor is exposed from aggrecan degradation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the pro-inflammatory cytokines associated with OA?

A

IL-1
IL-6
TNF alpha
IF gamma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How do the pro-inflammatory cytokines drive the breakdown of cartilage?

A
  1. modulate chondrocyte metabolism to increase MMP synthesis
  2. inhibiting synthesis of MMP inhibitory molecules
  3. inhibiting synthesis of collagen and proteoglycans
  4. inducing chondrocytes to increase PGE2, NO, etc to affect matrix synthesis and degradation
16
Q

What is the result of cartilage breakdown?

A

Changes in subchondral bone

  • osteoclasts and osteoblasts
  • thickening of sub-chondral plate

Osteophytes form near cartilage loss

Synovium becomes edematous and inflammed

17
Q

What are the common sites for OA?

A

Non-symmetrical:

  • neck
  • lumbar spine
  • hip
  • fingers
  • knee
18
Q

What are the mediators of pain in OA?

A
  • VIP
  • TRPV1
  • NO
  • NGF
  • prostagladins
19
Q

What causes pain in OA?

Cartilage loss or osteophytes?

A

NOT cartilage loss, cartilage has no innervation

Bones spurs can cause pain though

20
Q

What are some non-pharm treatments of OA?

A
  • weight loss
  • patient education
  • exercise
  • PT
  • braces
  • physical modalities (treatment tools used by therapists)
21
Q

What are 2 functions of the synovial fluid in the joint?

A
  • lubrication

- viscosity