MSK Module 2 Flashcards
(69 cards)
1
Q
Synovial joint is composed of:
A
- Joint capsule (fibrous + synovial membrane)
- Joint space
- Synovial fluid
- Articular cartilage
2
Q
Outer layer of the joint capsule and what it consists of:
A
- Fibrous capsule (connective tissue)
- Poor blood supply
- Rich in joint (sensory) receptors
3
Q
Inner layer of joint capsule and what it consists of:
A
- Synovium
- Type A and B cells
4
Q
Type A cells of synovium in joint capsule:
A
Immune function
5
Q
Type B cells of synovium in joint capsule:
A
Synovial fluid production
- Secrete HA to improve viscosity of fluid
- Secrete lubricin to reduce friction in joint
6
Q
What does synovial fluid contain?
A
- Hyaluronic acid (HA)
- Lubricin
- Proteinases
- Collagenases
7
Q
Define thixotropic properties
A
Viscosity of synovial fluid varies inversely with velocity of movement
8
Q
Define articular cartilage and its functions
A
- Thin hyaline covering on the ends of most bones
- Reduces friction
- Absorbs/disperses compressive forces
9
Q
What is articular cartilage composed of?
A
- Cell component: chondrocytes
- EC matrix (non fibrous and fibrous)
10
Q
What are chondrocytes and their functions?
A
- Cellular component of articular cartilage
- Produce and maintain EC matrix
- Forms 2% of cartilage
11
Q
Describe the EC matrix of articular cartilage
A
- Non fibrous: regulates fluid flow in/out, consists of water (mainly) and proteins
- Fibrous (10-30% of cartilage): Type 2 collagen arranged to absorb mechanical stress
12
Q
Describe the zones of the cartilage-bone interface
A
- Zone 1: smooth outer layer, reduces friction
- Zones 2 and 3: transitional, absorb compressive forces
- Tidemark: b/w uncalcified and calcified layers
- Zone 4: calcified, anchors cartilage to bone
13
Q
What is the significance of EC matrix turnover?
A
Optimal joint function requires consistent matrix turnover
14
Q
How do hormones regulate matrix turnover? Which ones?
A
GH and IGF stimulate chondrocytes
15
Q
____ are responsible for regulating fluid flow in/out of cartilage
A
Proteoglycans
16
Q
The more cartilage is compressed, fluid flow becomes slower and resistance becomes _____
A
Exponentially harder
17
Q
Describe the nerve/blood supply of articular cartilage
A
- NONE
- Pain insensitive
- Poor healing
18
Q
What is the MC joint disease?
A
Osteoarthritis
19
Q
Define osteoarthritis
A
Classified as “non-inflammatory”, however evidence suggests an inflammatory component
20
Q
What is the primary defect of osteoarthritis? What are the gross changes?
A
- Loss/disruption of articular cartilage
- Smooth glossy surface becomes a dull yellow/brown with flaking fissures
21
Q
What are the enzymatic changes of osteoarthritis?
A
- Excessive enzyme secretion by chondrocytes leading to EC matrix breakdown
- Proteoglycans are broken down leading to fluid disruption
22
Q
What are the hormonal changes of osteoarthritis?
A
Chondrocytes become less sensitive to GH/IGF
23
Q
What are the cytokine effects in osteoarthritis?
A
-Excessive production of IL-1 leads to inhibition of normal cytokine regulation of matrix turnover-IL-1 facilitates NO synthesis
24
Q
What are the NO effects in osteoarthritis?
A
- NO not normally found in healthy joint (found in OA synovium)
- NO facilitates chondrocyte death (apoptosis)
25
How do fluid changes occur within articular cartilage in OA?
- At rest (non wt bearing): increased volume within cartilage
- Wt bearing: fluid pushed out rapidly and cartilage is easily compressed w/o much resistance (oppo in healthy)
- Net result: cartilage has limited ability to absorb forces and provide adequate nutrients to chondrocytes
26
How does OA affect surrounding structures (not articular cartilage)?
- Subchondral bone sclerosis and bone cysts
- Osteophyte formation
- Synovial thickening
27
Etiology of OA
Multifactorial
- Trauma
- Genetics
- Other (inflamm conditions, neuro disorders, joint/ligament laxity)
28
How does exercise affect risk of developing OA?
- Low impact has low or NO risk
| - High impact tends to increase risk d/t traumatic forces/injuries
29
Where are Heberden's nodes located?
DIP joint in OA
30
Where are Bouchard's nodes located?
PIP joint in OA
31
Clinical manifestations of OA
- Morning pain
- Pain following prolonged postural positions
- Referred pain
- Joint deformation
- Loss of function/mobility
32
Treatment of OA
- Conservative
- Pharma
- Surgical
33
What are the surgical methods of treating OA?
- Viscosupplementation
- Cartilage "repair" strategies
- Arthroplasty (joint replacement)
34
What is viscosupplementation?
- Tx method of OA
- Hyaluronan injection to improve viscous properties of synovial fluid
- FDA approved for knee only
35
What are the different cartilage repair strategies for treating OA?
- Lavage and debridement*
- Microfracture (marrow stimulating)
- OATS (osteochondral auto and allografts)
- Autologous chondrocyte implantation
* Technically not a "repair"
36
Describe arthroscopic lavage and debridement
- Tx option for OA
- Not technically a repair
- Short term to relieve symps
- Lavage (clean/wash out), debride (remove flakes or rough areas)
37
Describe the marrow stimulating techniques for treating OA?
- Aka microfracture
- Removal of damaged cartilage to expose underlying bone
- Expose blood vessels
- Fibrocartilage fills defect
38
Describe osteochondral autograft
- Tx for OA
| - Graft comes from patient (usually non-wt bearing area of knee)
39
Describe osteochondral allograft
- Tx for OA
- Graft comes from other person/cadaver
- Allows more tissue to be taken so larger areas of defect can be repaired
40
Describe autologous chondrocyte implantation
- Tx for OA
- Phase 1: small sample taken to "grow" chondrocytes for 3-6 wks
- Phase 2: chondral defect is prepared and cells planted
* Expensive!
41
Describe arthroplasty
- Last resort tx for OA
| - Elective: determined by pain and quality of life
42
What is non-infectious inflammatory joint disease?
Inflammation due to autoimmune reactions
43
What is RA and what are the primary/secondary tissues involved?
- Systemic autoimmune, chronic inflamm of CT in joints primarily
- Primary tissue: synovial membrane
- Secondary tissues: articular cartilage, fibrous joint capsule, menisci, etc.
44
What are the MC joints involved in RA?
Fingers, wrist, elbow
| Knee, ankle, foot
45
What is rheumatoid factor?
- Autoantibody
| - Combines with IgM, IgG and IgA as autoimmune complexes that are deposited in joint tissue
46
In RA, which components of synovial fluid are activated?
- CD4 T helper cells
| - B lymphocytes
47
Role of B lymphocytes in RA?
-Facilitates formation of RF (rheumatoid factor)
48
What happens to the autoimmune complexes in RA?
Macrophages consume them and release lytic enzymes that destroy synovium
49
Role of CD4 T helpers in RA?
- Facilitate release of inflammatory enzymes that destroy joint structures
- Facilitate release of RANKL which promotes osteoclast activity
50
What is a Z deformity in RA?
Radial deviation of the wrist with ulnar deviation of the fingers
51
What is a "swan neck" deformity in RA?
Extended PIP with flexed DIP
52
What is a boutonniere deformity in RA?
Flexed PIP with extended DIP?
53
What is a pannus formation?
"Cloth cover"
| -Granulation (scar) tissue covers articular surfaces in RA
54
What do extra-articular manifestations of RA indicate?
Increased mortality rate and more severe disability
55
What is the MC ocular complication of RA?
Scleritis
| poor prognosis
56
Examples of extra-articular manifestations of RA
- Extrasynovial nodules (MC elbows, fingers)
- Neuropathies
- Amyloid in kidneys
- Vasculitis
57
What is Felty's syndrome?
- Extra-articular manifestation of RA
| - Consists of anemia, splenomegaly, leukopenia
58
What are the 3 forms of juvenile RA?
1. Pauciarticular (Mildest and MC, 1-4 joints)
2. Polyarticular (Moderate, 4+ joints)
3. Systemic (Most severe but least common)
59
What makes juvenile RA different than adult RA?
1. Antinuclear antibodies (ANA) present while RF usually isn't
2. Large joints
3. More often involves C-spine
60
What causes gout and which populations are MC affected?
- Hyperuricemia
| - Males, 30-50 yo onset
61
Uric acid is the end product of:
Purine metabolism
62
Pathophys of hyperuricemia
- Uric acid deposits in connective tissues surrounding joints
- Saturates synovial fluid and crystallizes
- Crystals provoke inflammatory response
63
What is a tophus?
Subcutaneous deposit of uric acid crystals (from chronic elevation of uric acid)
64
Chronic elevation of uric acid forms:
Tophus (SC deposits of crystals)
65
Which joint is almost always the first attack of gout?
MTP of big toe
66
How long do gout attacks last and how do they resolve?
-2-3 days
-Spontaneous remission
(attacks get closer together as disease progresses)
67
What is ankylosing spondylitis and what is the etiology?
- Chronic inflammatory joint disease
- Results in stiffening and fusion of spine and SI joint
- A/w HLA-B27
68
Classic vs. recent theories of ankylosing spondylitis pathophys
- Classic theories suggest destruction occurs at enthesis (attachment sites of tendons, ligaments, joint capsule)
- New theories suggest cartilage and other structures are initial target of inflammatory response
69
What causes fusion of spine to SI joint in ankylosing spondylitis?
- Inflammatory response causes reparative reaction from fibroblasts
- Fibroblasts secrete collagen forming "scar tissue" which calcifies and results in fusion
