Test 2: lecture 18 osteoarthritis Flashcards

1
Q

Progressive articular cartilage degradation without adequate repair

A

osteoarthritis

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

OA that develops after known trauma

A

Posttraumatic Osteoarthritis (PTOA)

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

OA will do what to the joint

A

synovitis
mediscal degeneration and tear
osteophyotosis
loss of collagen
sub-condral bone sclerosis

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

Synovial fluid is ultrafiltrate of plasma providing— and —

A

nutrients & lubrication

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

subchondral bone is — bone deep to cartilage and will—

A

cortical

absorb force acting on the joint

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what type of cartilage in the joints

A

hyaline/articular cartilage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

articular cartilage is made by — cell types

A

chondrocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

why can’t articular cartilage heal well?

A

avascular and aneural
limited intrinsic repair

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

ECM of articular cartilage is made of

A

95%: type 2 collagen
proteoglycans (aggrecan)
glycoproteins
hyaluronan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

ECM of articular cartilage is maintained by

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

cartilage trauma causes increase in —

A

inflammation
ECM degradation
apoptosis
posttraumatic inflammation (IL-1β, TNF⍺, MMPs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what are the main catabolic cytokine

A

IL-1β, TNFα, IL-17

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are the main degradtative enzymes

A

MMPs, ADAMTS

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

joint injury causes stress activation of — and —

A

chondrocytes
synoviocytes

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

MMPs will —

A

breakdown collagen fibers
(collagenases)

type of degradative enzyme

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

ADAMTs will —

A

cause break down of proteoglycans (aggrecan)

“aggrecanases”

type of degradative enzyme: MMPs, ADAMTS

17
Q

what happens to sub chondral bone if articular surface is lost

A

degrades: sclerotic and eburnated

18
Q

how to diagnose OA

A

lameness exam/ pain
diagnostic analgesia
Radiography
Ultrasonography, MRI, CT, PET
Diagnostic arthroscopy

19
Q

what is a positive flexion test

A

if you hold joint in flexion, then let it go lameness will be worse

20
Q

joint distension vs joint enlargement

A

distension: from increased fluid and inflammation

enlargement: thickening of joint capsule and bony spurs (osteophyte)

21
Q

ankylosis

A

abnormal stiffening and immobility of a joint due to fusion of the bones.

22
Q

what is seen on Xray of OA

A

osteophytes
Joint space narrowing / asymmetry
Subchondral sclerosis
Subchondral lysis
Osteochondral fragments
Ankylosis

23
Q

what causes swollen joints to be painfull?

A

damage to subchondral bone

joint capsule: pressure from increased fluid, thick capsule can reduce mobility

24
Q

4 conservative treatments of OA

A
  • Systemic medications
  • Intra-articular injections
  • Controlled exercise
  • Weight loss
25
Q

4 surgical treatments of OA

A
  • Resurface cartilage defects
  • Remove osteochondral fragments
  • Total joint replacement
  • Arthrodesis
26
Q

what are some meds that can be used for OA

A

NSAIDs
steroids
hyaluronic acid
PSGAGs

27
Q

hyaluronic acid will — joints.

A

lubricate and antiinflammatory

  • will cause joint to make more HA from type B synoviocytes
  • acts as anti-inflammatory: blocks PGE2 and free radicals and prevents cell migration

injected directly into joint

28
Q

what does PSGAGs do?

A

stimulates EMC matrix synthesis (type 2 collagen and protegylcans)

inhibits MMPs
promotes HA synthesis (lubricate and anti-inflammatory)
Anti-inflammatory: blocks PGE2 and free radicals

Adequan

29
Q

PSGAG will inhibit?

A

MMPs (which degrade collagen fibers)

inhibits PGE2 and free radicals (acts as anti-inflammatory)

Adequan:
increases HA synthesis and stimulated matrix synthesis: type 2 collagen and proteglycans

30
Q

polyacrylamide hydrogels will —

A

lubricate joint
analagesic effect on joint- incoporates into the synovial membrane (change elasticity)

noltex, arthramid: intra-articular injection
NON degradable

31
Q

— is a non degradable intra articular injection to increase lubrication and reduce pain in joint

A

polyacrylamide hydrogel
Noltrex (USA), Arthramid (Europe)

32
Q

complications of joint injections

A

joint flare: acute inflammatory response

Joint infection: septic arthritis- needs aggressive treatment

33
Q

Autologous conditioned serum is used for —

A

block IL-1

made from self and acts as anti-inflammatory

interleukin-1 antagonist protein (IRAP)

34
Q

— is a competitive antagonism of IL-1 made from incubate autologous blood

A

Autologous conditioned serum (ACS)

interleukin-1 antagonist protein (IRAP)

35
Q

what is PRP

A

platelet rich plasma

plateletes have high concentration of growth factors : PDGF, TGF-β, FGF, VEGF

will promote healing, cell proliferation, matrix synthesis and angiogenesis

36
Q

what will platelet rich plasma do?

A

will promote healing, cell proliferation, matrix synthesis and angiogenesis

Platelets contain high concentration of growth factors
* PDGF, TGF-β, FGF, VEGF, EGF